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  • 1.
    Abelius, Martina
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Jedenfalk, Malin
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Ernerudh, Jan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Immunology and Transfusion Medicine.
    Janefjord, Camilla
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Berg, Göran
    Linköping University, Department of Clinical and Experimental Medicine, Division of Children's and Women's health. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Gynaecology and Obstetrics in Linköping.
    Matthiesen, Leif
    Linköping University, Department of Clinical and Experimental Medicine, Division of Children's and Women's health. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Gynaecology and Obstetrics in Linköping. Helsingborg Hospital, Sweden.
    Jenmalm, Maria
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Pregnancy modulates the allergen-induced cytokine production differently in allergic and non-allergic women2017In: Pediatric Allergy and Immunology, ISSN 0905-6157, E-ISSN 1399-3038, Vol. 28, no 8, p. 818-824Article in journal (Refereed)
    Abstract [en]

    Background: The immunological environment during pregnancy may differ between allergic and non-allergic women. This study investigates the effect of maternal allergy on the allergen-induced cytokine and chemokine levels and whether pregnancy modulates these immune responses differently in allergic and non-allergic women. Methods: The birch-, cat-, phytohemagglutinin- and tetanus toxoid-induced interferon-gamma(IFN-gamma), interleukin (IL)-4, IL-5, IL-10, IL-13, the T-helper 1 (Th1)-associated chemokine CXCL10 and the Th2-associated chemokine CCL17 levels were quantified in 20 women with allergic symptoms (sensitized, n=13) and 36 women without allergic symptoms (non-sensitized, n=30) at gestational weeks 10-12, 15-16, 25, 35 and 2 and 12months post-partum. Results: Birch-, but not cat-induced, IL-5, IL-13 and CCL17 levels were increased during pregnancy as compared to post-partum in the sensitized women with allergic symptoms. In contrast, cat-, but not birch-induced, IL-5 and IL-13 levels were increased during pregnancy as compared to post-partum in the non-sensitized women without allergic symptoms. Furthermore, IFN-gamma secretion was increased in the first and decreased in the second and third trimesters in response to birch and decreased in the third trimester in response to cat as compared to post-partum in the non-sensitized women without allergic symptoms. Increased allergen-induced IL-4, IL-5 and IL-13 levels were associated with allergic symptoms and sensitization. Conclusions: Pregnancy had a clear effect on the allergen-induced IL-5, IL-13, CCL17, IFN-gamma and CXCL10 production, with distinct enhanced Th2-responses to birch in the allergic group and to cat in the non-allergic group.

  • 2.
    Ahlbeck, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Astma lathund: Astma hos vuxna2018Other (Other academic)
    Abstract [sv]

    Åtta till tio procent av den vuxna befolkningen har astma. Av dessa har65 procent lindrig, 25 procent medelsvår och 10 procent svår astma.Astma är en heterogen sjukdom, där en kronisk luftvägsinflammationoftast föreligger.

    Sjukdomen kännetecknas av återkommande luftvägssymtom såsom pipi bröstet, andnöd, trånghetskänsla i bröstet och hosta som varierar övertiden tillsammans med en variabel luftvägsobstruktion.

  • 3.
    Ahlbeck, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Allergy Center.
    Astmainhalator med återkopplingssystem gav bättre vård och sänkta kostnader [Asthma inhaler with feedback system provided better care and lower costs].2014In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 111, no 5, p. 160-160Article in journal (Other academic)
  • 4.
    Ali, Neserin
    et al.
    Lund Univ, Sweden.
    Ljunggren, Stefan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center.
    Karlsson, Helen
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center.
    Wierzbicka, Aneta
    Lund Univ, Sweden.
    Pagels, Joakim
    Lund Univ, Sweden.
    Isaxon, Christina
    Lund Univ, Sweden.
    Gudmundsson, Anders
    Lund Univ, Sweden.
    Rissler, Jenny
    Lund Univ, Sweden.
    Nielsen, Jorn
    Lund Univ, Sweden.
    Lindh, Christian H.
    Lund Univ, Sweden.
    Karedal, Monica
    Lund Univ, Sweden.
    Comprehensive proteome analysis of nasal lavage samples after controlled exposure to welding nanoparticles shows an induced acute phase and a nuclear receptor, LXR/RXR, activation that influence the status of the extracellular matrix2018In: Clinical Proteomics, ISSN 1542-6416, E-ISSN 1559-0275, Vol. 15, article id 20Article in journal (Refereed)
    Abstract [en]

    Background: Epidemiological studies have shown that many welders experience respiratory symptoms. During the welding process a large number of airborne nanosized particles are generated, which might be inhaled and deposited in the respiratory tract. Knowledge of the underlying mechanisms behind observed symptoms is still partly lacking, although inflammation is suggested to play a central role. The aim of this study was to investigate the effects of welding fume particle exposure on the proteome expression level in welders suffering from respiratory symptoms, and changes in protein mediators in nasal lavage samples were analyzed. Such mediators will be helpful to clarify the pathomechanisms behind welding fume particle-induced effects. Methods: In an exposure chamber, 11 welders with work-related symptoms in the lower airways during the last month were exposed to mild-steel welding fume particles (1 mg/m(3)) and to filtered air, respectively, in a double-blind manner. Nasal lavage samples were collected before, immediately after, and the day after exposure. The proteins in the nasal lavage were analyzed with two different mass spectrometry approaches, label-free discovery shotgun LC-MS/MS and a targeted selected reaction monitoring LC-MS/MS analyzing 130 proteins and four in vivo peptide degradation products. Results: The analysis revealed 30 significantly changed proteins that were associated with two main pathways; activation of acute phase response signaling and activation of LXR/RXR, which is a nuclear receptor family involved in lipid signaling. Connective tissue proteins and proteins controlling the degradation of such tissues, including two different matrix metalloprotease proteins, MMP8 and MMP9, were among the significantly changed enzymes and were identified as important key players in the pathways. Conclusion: Exposure to mild-steel welding fume particles causes measurable changes on the proteome level in nasal lavage matrix in exposed welders, although no clinical symptoms were manifested. The results suggested that the exposure causes an immediate effect on the proteome level involving acute phase proteins and mediators regulating lipid signaling Proteases involved in maintaining the balance between the formation and degradation of extracellular matrix proteins are important key proteins in the induced effects.

  • 5.
    Ali, Neserin
    et al.
    Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden.
    Mattsson, Karin
    Center for Molecular Protein Science, Biochemistry and Structural Biology, Lund University, Lund, Sweden.
    Rissler, Jenny
    Department of Design Sciences, Ergonomic and Aerosol Technology, Lund University, Lund, Sweden.
    Karlsson, Helen Marg
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center.
    Svensson, Christian R
    Department of Design Sciences, Ergonomic and Aerosol Technology, Lund University, Lund, Sweden.
    Gudmundsson, Anders
    Department of Design Sciences, Ergonomic and Aerosol Technology, Lund University, Lund, Sweden.
    Lindh, Christian H
    Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden.
    Jönsson, Bo A G
    Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden.
    Cedervall, Tommy
    Center for Molecular Protein Science, Biochemistry and Structural Biology, Lund University, Lund, Sweden.
    Kåredal, Monica
    Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden.
    Analysis of nanoparticle-protein coronas formed in vitro between nanosized welding particles and nasal lavage proteins.2016In: Nanotoxicology, ISSN 1743-5390, E-ISSN 1743-5404, Vol. 10, no 2, p. 226-234Article in journal (Refereed)
    Abstract [en]

    Welding fumes include agglomerated particles built up of primary nanoparticles. Particles inhaled through the nose will to some extent be deposited in the protein-rich nasal mucosa, and a protein corona will be formed around the particles. The aim was to identify the protein corona formed between nasal lavage proteins and four types of particles with different parameters. Two of the particles were formed and collected during welding and two were manufactured iron oxides. When nasal lavage proteins were added to the particles, differences were observed in the sizes of the aggregates that were formed. Measurements showed that the amount of protein bound to particles correlated with the relative size increase of the aggregates, suggesting that the surface area was associated with the binding capacity. However, differences in aggregate sizes were detected when nasal proteins were added to UFWF and Fe2O3 particles (having similar agglomerated size) suggesting that yet parameters other than size determine the binding. Relative quantitative mass spectrometric and gel-based analyses showed differences in the protein content of the coronas. High-affinity proteins were further assessed for network interactions. Additional experiments showed that the inhibitory function of secretory leukocyte peptidase inhibitor, a highly abundant nasal protein, was influenced by particle binding suggesting that an understanding of protein function following particle binding is necessary to properly evaluate pathophysiological events. Our results underscore the importance of including particles collected from real working environments when studying the toxic effects of particles because these effects might be mediated by the protein corona.

  • 6.
    Baumann, Katrine Y.
    et al.
    RefLab ApS, Denmark; Univ Copenhagen, Denmark.
    Church, Martin K.
    Charite Univ Med Berlin, Germany.
    Clough, Geraldine F.
    Univ Southampton, England.
    Quist, Sven Roy
    Otto von Guericke Univ, Germany; Skin Ctr MDZ, Germany.
    Schmelz, Martin
    Heidelberg Univ, Germany.
    Skov, Per Stahl
    Odense Univ Hosp, Denmark.
    Anderson, Chris
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology.
    Tannert, Line Kring
    Odense Univ Hosp, Denmark.
    Gimenez-Arnau, Ana Maria
    Univ Autonoma Barcelona, Spain.
    Frischbutter, Stefan
    Charite Univ Med Berlin, Germany.
    Scheffel, Joerg
    Charite Univ Med Berlin, Germany.
    Maurer, Marcus
    Charite Univ Med Berlin, Germany.
    Skin microdialysis: methods, applications and future opportunities-an EAACI position paper2019In: Clinical and Translational Allergy, ISSN 2045-7022, E-ISSN 2045-7022, Vol. 9, article id 24Article, review/survey (Refereed)
    Abstract [en]

    Skin microdialysis (SMD) is a versatile sampling technique that can be used to recover soluble endogenous and exogenous molecules from the extracellular compartment of human skin. Due to its minimally invasive character, SMD can be applied in both clinical and preclinical settings. Despite being available since the 1990s, the technique has still not reached its full potential use as a tool to explore pathophysiological mechanisms of allergic and inflammatory reactions in the skin. Therefore, an EAACI Task Force on SMD was formed to disseminate knowledge about the technique and its many applications. This position paper from the task force provides an overview of the current use of SMD in the investigation of the pathogenesis of chronic inflammatory skin diseases, such as atopic dermatitis, chronic urticaria, psoriasis, and in studies of cutaneous events during type 1 hypersensitivity reactions. Furthermore, this paper covers drug hypersensitivity, UVB-induced- and neurogenic inflammation, and drug penetration investigated by SMD. The aim of this paper is to encourage the use of SMD and to make the technique easily accessible by providing an overview of methodology and applications, supported by standardized operating procedures for SMD in vivo and ex vivo.

  • 7.
    Bousquet, J.
    et al.
    CHRU, France; MACVIA LR, France; INSERM, France; University of Versailles St Quentin En Yvelines, France.
    Farrell, J.
    Department Health Social Serv and Public Safety, North Ireland.
    Crooks, G.
    Scottish Centre Telehealth and Telecare, Scotland.
    Hellings, P.
    Katholieke University of Leuven, Belgium; European Academic Allergy and Clin Immunol, Switzerland.
    Bel, E. H.
    University of Amsterdam, Netherlands; European Resp Soc, Switzerland.
    Bewick, M.
    iQ4U Consultants Ltd, England.
    Chavannes, N. H.
    Leiden University, Netherlands; Global Alliance Chron Resp Disease GARD, South Africa; Int Primary Care Resp Grp, Scotland.
    Correia de Sousa, J.
    University of Minho, Portugal.
    Cruz, A. A.
    Global Alliance Chron Resp Disease GARD, South Africa; University of Federal Bahia, Brazil; GARD Execut Comm, Brazil.
    Haahtela, T.
    EIP AHA Commitment Act, Portugal; Helsinki University Hospital, Finland.
    Joos, G.
    Ghent University Hospital, Belgium.
    Khaltaev, N.
    Global Alliance Chron Resp Disease GARD, South Africa.
    Malva, J.
    University of Coimbra, Portugal; Ageing Coimbra Reference Site, Portugal.
    Muraro, A.
    European Academic Allergy and Clin Immunol, Switzerland; Padua Gen University Hospital, Italy.
    Nogues, M.
    CARSAT LR, France.
    Palkonen, S.
    EFA European Federat Allergy and Airways Disease Patien, Belgium.
    Pedersen, S.
    University of Southern Denmark, Denmark.
    Robalo-Cordeiro, C.
    Coimbra University Hospital, Portugal.
    Samolinski, B.
    Medical University of Warsaw, Poland.
    Strandberg, T.
    University of Helsinki, Finland; University of Oulu, Finland; EUGMS, Norway.
    Valiulis, A.
    Vilnius University, Lithuania; European Assoc Pediat EAP UEMS SP, Belgium.
    Yorgancioglu, A.
    Global Alliance Chron Resp Disease GARD, South Africa; EIP AHA Commitment Act, Portugal; Celal Bayar University, Turkey; Turkish Thorac Soc, Turkey.
    Zuberbier, T.
    Charite, Germany; GA2LEN, Germany.
    Bedbrook, A.
    MACVIA LR, France.
    Aberer, W.
    Medical University of Graz, Austria.
    Adachi, M.
    Sanno Hospital, Japan.
    Agusti, A.
    University of Barcelona, Spain; CIBER Enfermedades Resp, Spain.
    Akdis, C. A.
    University of Zurich, Switzerland.
    Akdis, M.
    University of Zurich, Switzerland.
    Ankri, J.
    INSERM, France; University of Versailles St Quentin En Yvelines, France.
    Alonso, A.
    University of Barcelona, Spain; CIBER Enfermedades Resp, Spain.
    Annesi-Maesano, I.
    European Assoc Pediat EAP UEMS SP, Belgium; INSERM, France.
    Ansotegui, I. J.
    Hospital Quiron Bizkaia, Spain.
    Anto, J. M.
    Centre Research Environm Epidemiol CREAL, Spain; Hospital del Mar, Spain; CIBERESP, Spain; UPF, Spain.
    Arnavielhe, S.
    Digi Heatlh, France.
    Arshad, H.
    David Hide Asthma and Allergy Research Centre, England.
    Bai, C.
    Chinese Medical Assoc, Peoples R China; Chinese Alliance Lung Canc, Peoples R China.
    Baiardini, I.
    University of Genoa, Italy.
    Bachert, C.
    Ghent University Hospital, Belgium.
    Baigenzhin, A. K.
    EuroAsian Resp Soc, Kazakhstan.
    Barbara, C.
    Fac Medical Lisbon, Portugal.
    Bateman, E. D.
    University of Cape Town, South Africa.
    Beghe, B.
    University of Modena and Reggio Emilia, Italy.
    Ben Kheder, A.
    Hop Abderrahman Mami, Tunisia.
    Bennoor, K. S.
    National Institute Disease Chest and Hospital, Bangladesh.
    Benson, Mikael
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Bergmann, K. C.
    Charite, Germany; GA2LEN, Germany.
    Bieber, T.
    Rheinische Friedrich Wilhelms University of Bonn, Germany.
    Bindslev-Jensen, C.
    Odense University Hospital, Denmark; Odense University Hospital, Denmark.
    Bjermer, L.
    University Hospital, Sweden.
    Blain, H.
    Montpellier University Hospital, France; University of Montpellier, France.
    Blasi, F.
    University of Milan, Italy.
    Boner, A. L.
    University of Verona Hospital, Italy.
    Bonini, M.
    Sapienza University of Rome, Italy.
    Bonini, S.
    University of Naples 2, Italy; Italian National Research Council, Italy.
    Bosnic-Anticevitch, S.
    University of Sydney, Australia; Sydney Local Health Dist, Australia.
    Boulet, L. P.
    University of Laval, Canada.
    Bourret, R.
    Montpellier University Hospital, France.
    Bousquet, P. J.
    INSERM, France.
    Braido, F.
    University of Genoa, Italy.
    Briggs, A. H.
    University of Glasgow, Scotland.
    Brightling, C. E.
    University Hospital Leicester NHS Trust, England; University of Leicester, England.
    Brozek, J.
    McMaster University, Canada.
    Buhl, R.
    Johannes Gutenberg University of Mainz, Germany.
    Burney, P. G.
    Imperial Coll, England; Imperial Coll, England; Imperial Coll, England.
    Bush, A.
    Imperial Coll, England; Royal Brompton Hospital, England.
    Caballero-Fonseca, F.
    Centre Medical Docente Trinidad, Venezuela.
    Caimmi, D.
    Montpellier University Hospital, France.
    Calderon, M. A.
    Royal Brompton Hospital NHS, England.
    Calverley, P. M.
    University of Liverpool, England; Aintree University Hospital NHS Fdn Trust, England.
    Camargos, P. A. M.
    University of Federal Minas Gerais, Brazil.
    Canonica, G. W.
    University of Genoa, Italy.
    Camuzat, T.
    Regional Languedoc Roussillon, France.
    Carlsen, K. H.
    Oslo University Hospital, Norway; University of Oslo, Norway; Oslo University Hospital, Norway; University of Oslo, Norway.
    Carr, W.
    Allergy and Asthma Associates Southern Calif, CA USA.
    Carriazo, A.
    Regional Minist Equal Health and Social Policies Andalusia, Spain.
    Casale, T.
    University of S Florida, FL USA.
    Cepeda Sarabia, A. M.
    University of Simon Bolivar, Colombia; Soc Latinoamer Allergia, Colombia.
    Chatzi, L.
    University of Crete, Greece.
    Chen, Y. Z.
    Peking and Centre Asthma Research and Educ, Peoples R China; Peking and Centre Asthma Research and Educ, Peoples R China.
    Chiron, R.
    Montpellier University Hospital, France.
    Chkhartishvili, E.
    Grigol Robakidze University, Rep of Georgia.
    Chuchalin, A. G.
    GARD Execut Comm, Brazil; FMBA, Russia.
    Chung, K. F.
    Imperial Coll, England.
    Ciprandi, G.
    IRCCS Azienda Osped University of San Martino, Italy.
    Cirule, I.
    Latvian Allergy Assoc, Latvia.
    Cox, L.
    Nova Southeastern University, FL USA.
    Costa, D. J.
    MACVIA LR, France; Leiden University, Netherlands.
    Custovic, A.
    Imperial Coll London, England.
    Dahl, R.
    Odense University Hospital, Denmark; Odense University Hospital, Denmark.
    Dahlen, S. E.
    Karolinska Institute, Sweden.
    Darsow, U.
    Technical University of Munich, Germany; Technical University of Munich, Germany.
    De Carlo, G.
    EFA European Federat Allergy and Airways Disease Patien, Belgium.
    De Blay, F.
    University Hospital Strasbourg, France.
    Dedeu, T.
    European Regional and Local Health Assoc, Belgium; University of Edinburgh, Scotland.
    Deleanu, D.
    Iuliu Hatieganu University of Medical and Pharm, Romania.
    De Manuel Keenoy, E.
    Kronikgune, Spain.
    Demoly, P.
    INSERM, France; Montpellier University Hospital, France.
    Denburg, J. A.
    McMaster University, Canada.
    Devillier, P.
    Suresnes University of Versailles St Quentin, France.
    Didier, A.
    Rangueil Larrey Hospital, France.
    Dinh-Xuan, A. T.
    University of Paris 05, France.
    Djukanovic, R.
    University of Southampton, England.
    Dokic, D.
    University of Clin Pulmol and Allergy, Macedonia.
    Douagui, H.
    Centre Hospital University of Beni Messous, Algeria.
    Dray, G.
    Ecole Mines, France.
    Dubakiene, R.
    Vilnius University, Lithuania.
    Durham, S. R.
    Imperial Coll London, England.
    Dykewicz, M. S.
    St Louis University, MO USA.
    El-Gamal, Y.
    Ain Shams University, Egypt.
    Emuzyte, R.
    Vilnius University, Lithuania.
    Fabbri, L. M.
    University of Modena, Italy.
    Fletcher, M.
    Educ Heatlh, England.
    Fiocchi, A.
    Bambino Gesu Childrens Research Hospital Holy See, Italy.
    Fink Wagner, A.
    GAAPP, Austria.
    Fonseca, J.
    University of Porto, Portugal; CUF Porto Institute and Hospital, Portugal.
    Fokkens, W. J.
    Academic Medical Centre, Netherlands.
    Forastiere, F.
    Regional Health Serv Lazio Reg, Italy.
    Frith, P.
    Repatriat Gen Hospital, Australia.
    Gaga, M.
    Athens Chest Hospital, Greece.
    Gamkrelidze, A.
    National Centre Disease Control and Public Health Georgia, Rep of Georgia.
    Garces, J.
    University of Valencia, Spain.
    Garcia-Aymerich, J.
    Centre Research Environm Epidemiol CREAL, Spain; Hospital del Mar, Spain; CIBERESP, Spain; UPF, Spain.
    Gemicioglu, B.
    Istanbul University, Turkey.
    Gereda, J. E.
    Clin Ricardo Palma, Peru.
    Gonzalez Diaz, S.
    University of Autonoma Nuevo Leon, Mexico.
    Gotua, M.
    Georgian Assoc Allergol and Clin Immunol, Rep of Georgia.
    Grisle, I.
    Latvian Assoc Allergists, Latvia.
    Grouse, L.
    Washington University, MO 63110 USA.
    Gutter, Z.
    University Hospital Olomouc, Czech Republic.
    Guzman, M. A.
    University of Chile, Chile.
    Heaney, L. G.
    Queens University of Belfast, North Ireland.
    Hellquist-Dahl, B.
    Odense University Hospital, Denmark.
    Henderson, D.
    Scottish Centre Telehealth and Telecare, Scotland.
    Hendry, A.
    NHS Scotland, Scotland.
    Heinrich, J.
    Helmholtz Zentrum Munchen, Germany.
    Heve, D.
    MACVIA LR, France; Agence Regional Sante, France.
    Horak, F.
    Vienna Challenge Chamber, Austria.
    Hourihane, J. O. B.
    University of Coll Cork, Ireland.
    Howarth, P.
    University of Southampton, England.
    Humbert, M.
    University of Paris Sud, France.
    Hyland, M. E.
    University of Plymouth, England.
    Illario, M.
    Federico II University Hospital Campania RS, Italy.
    Ivancevich, J. C.
    Clin Santa Isabel, Argentina.
    Jardim, J. R.
    University of Federal Sao Paulo, Brazil.
    Jares, E. J.
    Libra Fdn, Argentina.
    Jeandel, C.
    MACVIA LR, France; Montpellier University Hospital, France.
    Jenkins, C.
    University of Sydney, Australia.
    Johnston, S. L.
    Imperial Coll, England; MRC and Asthma UK Centre Allerg Mech Asthma, England.
    Jonquet, O.
    Montpellier University Hospital, France.
    Julge, K.
    Tartu University Hospital, Estonia.
    Jung, K. S.
    Hallym University, South Korea.
    Just, J.
    Hop Enfants Armand Trousseau, France; Sorbonne University, France.
    Kaidashev, I.
    Ukrainian Medical Stomatol Acad, Ukraine.
    Kaitov, M. R.
    Federal Medicobiol Agency, Russia.
    Kalayci, O.
    Hacettepe University, Turkey.
    Kalyoncu, A. F.
    Hacettepe University, Turkey.
    Keil, T.
    Charite, Germany; University of Wurzburg, Germany.
    Keith, P. K.
    McMaster University, Canada.
    Klimek, L.
    Centre Rhinol and Allergol, Germany.
    Koffi NGoran, B.
    Soc Pneumol Langue Francaise, France.
    Kolek, V.
    University Hospital Olomouc, Czech Republic.
    Koppelman, G. H.
    University of Groningen, Netherlands.
    Kowalski, M. L.
    Medical University of Lodz, Poland; HARC, Poland.
    Kull, I.
    Sachs Childrens Hospital, Sweden; Karolinska Institute, Sweden.
    Kuna, P.
    Medical University of Lodz, Poland.
    Kvedariene, V.
    Vilnius University, Lithuania.
    Lambrecht, B.
    University of Ghent, Belgium.
    Lau, S.
    Charite, Germany.
    Larenas-Linnemann, D.
    Hospital Medical Sur, Mexico.
    Laune, D.
    Digi Heatlh, France.
    Le, L. T. T.
    University of Medical and Pharm, Vietnam.
    Lieberman, P.
    University of Tennessee, TN USA; University of Tennessee, TN USA; University of Tennessee, TN USA; University of Tennessee, TN USA.
    Lipworth, B.
    University of Dundee, Scotland.
    Li, J.
    Guangzhou Medical University, Peoples R China.
    Lodrup Carlsen, K.
    Oslo University Hospital, Norway; University of Oslo, Norway; Oslo University Hospital, Norway; University of Oslo, Norway.
    Louis, R.
    CHU Sart Tilman, Belgium.
    MacNee, W.
    University of Edinburgh, Scotland.
    Magard, Y.
    Hop St Joseph, France.
    Magnan, A.
    University of Nantes, France; University of Nantes, France.
    Mahboub, B.
    Rashid Hospital, U Arab Emirates.
    Mair, A.
    Scottish Govt Health Department, Scotland.
    Majer, I.
    University of Bratislava, Slovakia.
    Makela, M. J.
    Helsinki University Hospital, Finland.
    Manning, P.
    Bon Secours Hospital, Ireland.
    Mara, S.
    AOU Citta Salute and Science Torino, Italy.
    Marshall, G. D.
    University of Mississippi, MS 39216 USA.
    Masjedi, M. R.
    Shahid Beheshti University of Medical Science, Iran.
    Matignon, P.
    VingCard Elsafe, Norway.
    Maurer, M.
    Charite, Germany.
    Mavale-Manuel, S.
    Maputo Central Hospital, Mozambique.
    Melen, E.
    Karolinska Institute, Sweden.
    Melo-Gomes, E.
    PNDR Portuguese National Programme Resp Disease, Portugal.
    Meltzer, E. O.
    Allergy and Asthma Medical Grp and Research Centre, CA USA.
    Menzies-Gow, A.
    Royal Brompton Hospital, England.
    Merk, H.
    Rhein Westfal TH Aachen, Germany.
    Michel, J. P.
    EUGMS, Norway.
    Miculinic, N.
    Croatian Pulm Soc, Croatia.
    Mihaltan, F.
    National Institute Pneumol M Nasta, Romania.
    Milenkovic, B.
    University of Belgrade, Serbia; Serbian Assoc Asthma, Serbia; COPD, Serbia.
    Mohammad, G. M. Y.
    Tishreen University, Syria.
    Molimard, M.
    University of Bordeaux, France.
    Momas, I.
    Paris Descartes University, France; Paris Municipal Department Social Act Childhood and Heatlh, France.
    Montilla-Santana, A.
    Aura Andalucia, Spain.
    Morais-Almeida, M.
    Hospital CUF Descobertas, Portugal.
    Morgan, M.
    NHS England, England.
    Mosges, R.
    University of Cologne, Germany.
    Mullol, J.
    Sachs Childrens Hospital, Sweden; Karolinska Institute, Sweden; Hospital Clin Barcelona, Spain.
    Nafti, S.
    Mustapha Hospital, Algeria.
    Namazova-Baranova, L.
    Russian Academic Medical Science, Russia.
    Naclerio, R.
    University of Chicago, IL 60637 USA; University of Chicago, IL 60637 USA.
    Neou, A.
    Charite, Germany; GA2LEN, Germany.
    Neffen, H.
    Hospital Ninos Orlando Alassia, Argentina.
    Nekam, K.
    Hospital Hospitaller Bros Buda, Hungary.
    Niggemann, B.
    Charite, Germany.
    Ninot, G.
    University of Montpellier I, France.
    Nyembue, T. D.
    University Hospital Kinshasa, DEM REP CONGO.
    OHehir, R. E.
    Monash University, Australia; Monash University, Australia; Monash University, Australia.
    Ohta, K.
    Tokyo National Hospital, Japan.
    Okamoto, Y.
    Chiba University Hospital, Japan.
    Okubo, K.
    Nippon Medical Sch, Japan.
    Ouedraogo, S.
    Centre Hospital University of Pediat Charles de Gaulle, Burkina Faso.
    Paggiaro, P.
    University Hospital Pisa, Italy.
    Pali-Scholl, I.
    University of Vet Med, Austria; Medical University, Austria.
    Panzner, P.
    Charles University of Prague, Czech Republic; Charles University of Prague, Czech Republic.
    Papadopoulos, N.
    University of Manchester, England; University of Athens, Greece.
    Papi, A.
    University of Ferrara, Italy.
    Park, H. S.
    Ajou University, South Korea.
    Passalacqua, G.
    University of Genoa, Italy.
    Pavord, I.
    University of Oxford, England.
    Pawankar, R.
    Nippon Medical Sch, Japan.
    Pengelly, R.
    Department Health Social Serv and Public Safety, North Ireland.
    Pfaar, O.
    Centre Rhinol and Allergol, Germany; Heidelberg University, Germany.
    Picard, R.
    Minist Econ Ind and Numer, France.
    Pigearias, B.
    Soc Pneumol Langue Francaise, France.
    Pin, I.
    CHU Grenoble, France.
    Plavec, D.
    University of JJ Strossmayer, Croatia.
    Poethig, D.
    Europe Europa Vereinigung Vitalitat and Aktives Alt, Germany.
    Pohl, W.
    Hietzing Hospital, Austria.
    Popov, T. A.
    Medical University of Sofia, Bulgaria.
    Portejoie, F.
    MACVIA LR, France.
    Potter, P.
    University of Cape Town, South Africa.
    Postma, D.
    University of Groningen, Netherlands.
    Price, D.
    University of Aberdeen, Scotland; Research Real Life, England.
    Rabe, K. F.
    German Centre Lung Research DZL, Germany; University of Kiel, Germany; German Centre Lung Research DZL, Germany.
    Raciborski, F.
    Medical University of Warsaw, Poland.
    Radier Pontal, F.
    Maison Profess Liberales, France.
    Repka-Ramirez, S.
    SLAAI, Colombia.
    Reitamo, S.
    Helsinki University Hospital, Finland.
    Rennard, S.
    University of Nebraska Medical Centre, NE USA.
    Rodenas, F.
    University of Valencia, Spain.
    Roberts, J.
    Salford Royal NHS Fdn Trust and NHS England North, England.
    Roca, J.
    University of Barcelona, Spain.
    Rodriguez Manas, L.
    Hospital University of Getafe Serv Madrileno Salud, Spain.
    Rolland, C.
    Assoc Asthme and Allergie, France.
    Roman Rodriguez, M.
    Institute Invest Sanitaria Palma IdisPa, Spain.
    Romano, A.
    Complesso Integrato Columbus, Italy.
    Rosado-Pinto, J.
    Hospital Luz, Portugal.
    Rosario, N.
    University of Parana, Brazil.
    Rosenwasser, L.
    Medical University of Misouri Kansas City, MO USA; Medical University of Misouri Kansas City, MO USA.
    Rottem, M.
    Emek Medical Centre, Israel.
    Ryan, D.
    Woodbrook Medical Centre, England; University of Edinburgh, Scotland.
    Sanchez-Borges, M.
    Centre Medicodocente Trinidad and Clin El Avila, Venezuela.
    Scadding, G. K.
    UCL, England.
    Schunemann, H. J.
    McMaster University, Canada.
    Serrano, E.
    CHU Rangueil Larrey, France.
    Schmid-Grendelmeier, P.
    University of Zurich Hospital, Switzerland.
    Schulz, H.
    Helmholtz Zentrum Munchen, Germany.
    Sheikh, A.
    University of Edinburgh, Scotland.
    Shields, M.
    Queens University of Belfast, North Ireland; Royal Belfast Hospital Sick Children, North Ireland.
    Siafakas, N.
    University Hospital Heraklion, Greece.
    Sibille, Y.
    Catholic University of Louvain, Belgium.
    Similowski, T.
    Sorbonne University, France; INSERM, France; Groupe, France.
    Simons, F. E. R.
    University of Manitoba, Canada.
    Sisul, J. C.
    Soc Paraguaya Alergia Asma and Inmunol, Paraguay.
    Skrindo, I.
    Oslo University Hospital, Norway; University of Oslo, Norway.
    Smit, H. A.
    University of Utrecht, Netherlands.
    Sole, D.
    University of Federal Sao Paulo, Brazil.
    Sooronbaev, T.
    Euro Asian Resp Soc, Kyrgyzstan.
    Spranger, O.
    GAAPP, Austria.
    Stelmach, R.
    University of Sao Paulo, Brazil.
    Sterk, P. J.
    University of Amsterdam, Netherlands.
    Sunyer, J.
    Centre Research Environm Epidemiol CREAL, Spain; CIBERESP, Spain; UPF, Spain.
    Thijs, C.
    Maastricht University, Netherlands.
    To, T.
    Sidkkids Hospital and Institute Health Policy Management and Eva, Canada.
    Todo-Bom, A.
    University of Coimbra, Portugal.
    Triggiani, M.
    University of Salerno, Italy.
    Valenta, R.
    Medical University of Vienna, Austria.
    Valero, A. L.
    Hospital Clin Barcelona, Spain.
    Valia, E.
    University of Valencia, Spain.
    Valovirta, E.
    University of Turku, Finland.
    Van Ganse, E.
    University of Claude Bernard, France.
    van Hage, M.
    Karolinska Institute, Sweden; University Hospital, Sweden.
    Vandenplas, O.
    Catholic University of Louvain, Belgium.
    Vasankari, T.
    Finnish Lung Assoc, Finland.
    Vellas, B.
    CHU Toulouse, France.
    Vestbo, J.
    University of Manchester, England; Manchester NHS Fdn Trust, England.
    Vezzani, G.
    Arcispedale S Maria Nuova, Italy; Regional Agency Health and Social Care, Italy.
    Vichyanond, P.
    Mahidol University, Thailand.
    Viegi, G.
    CNR, Italy; CNR, Italy.
    Vogelmeier, C.
    Philipps University of Marburg, Germany.
    Vontetsianos, T.
    Sotiria Hospital, Greece.
    Wagenmann, M.
    University of Klinikum Dusseldorf, Germany.
    Wallaert, B.
    CHRU, France.
    Walker, S.
    Asthma UK, England.
    Wang, D. Y.
    National University of Singapore, Singapore.
    Wahn, U.
    Charite, Germany.
    Wickman, M.
    Karolinska Institute, Sweden.
    Williams, D. M.
    University of N Carolina, NC USA.
    Williams, S.
    Int Primary Care Resp Grp, Scotland.
    Wright, J.
    Bradford Royal Infirm, England.
    Yawn, B. P.
    Olmsted Medical Centre, MN USA.
    Yiallouros, P. K.
    Cyprus University of Technology, Cyprus; Hospital Archbishop Makarios III, Cyprus.
    Yusuf, O. M.
    Allergy and Asthma Institute, Pakistan.
    Zaidi, A.
    University of Southampton, England.
    Zar, H. J.
    University of Cape Town, South Africa; University of Cape Town, South Africa.
    Zernotti, M. E.
    University of Catolica Cordoba, Argentina.
    Zhang, L.
    Capital Medical University, Peoples R China.
    Zhong, N.
    Guangzhou Medical University, Peoples R China.
    Zidarn, M.
    University of Clin Resp and Allerg Disease, Slovenia.
    Mercier, J.
    CHRU, France; University of Montpellier, France.
    Scaling up strategies of the chronic respiratory disease programme of the European Innovation Partnership on Active and Healthy Ageing (Action Plan B3: Area 5)2016In: Clinical and Translational Allergy, ISSN 2045-7022, E-ISSN 2045-7022, Vol. 6, article id 29Article, review/survey (Refereed)
    Abstract [en]

    Action Plan B3 of the European Innovation Partnership on Active and Healthy Ageing (EIP on AHA) focuses on the integrated care of chronic diseases. Area 5 (Care Pathways) was initiated using chronic respiratory diseases as a model. The chronic respiratory disease action plan includes (1) AIRWAYS integrated care pathways (ICPs), (2) the joint initiative between the Reference site MACVIA-LR (Contre les MAladies Chroniques pour un Vleillissement Actif) and ARIA (Allergic Rhinitis and its Impact on Asthma), (3) Commitments for Action to the European Innovation Partnership on Active and Healthy Ageing and the AIRWAYS ICPs network. It is deployed in collaboration with the World Health Organization Global Alliance against Chronic Respiratory Diseases (GARD). The European Innovation Partnership on Active and Healthy Ageing has proposed a 5-step framework for developing an individual scaling up strategy: (1) what to scale up: (1-a) databases of good practices, (1-b) assessment of viability of the scaling up of good practices, (1-c) classification of good practices for local replication and (2) how to scale up: (2-a) facilitating partnerships for scaling up, (2-b) implementation of key success factors and lessons learnt, including emerging technologies for individualised and predictive medicine. This strategy has already been applied to the chronic respiratory disease action plan of the European Innovation Partnership on Active and Healthy Ageing.

  • 8.
    Evaldsson, Chamilly
    Linköping University, Department of Clinical and Experimental Medicine, Clinical Chemistry. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Chemistry.
    Uridine, 4-thiouridine and isomaltitol in an asthma-like model: Anti-inflammatory and modulating effects2009Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    In chronic inflammatory diseases like asthma or rheumatoid arthritis, erroneous and exaggerated accumulation of leukocytes in a tissue inadvertently causes the body harm. Several efficient anti-inflammatory drugs exist, for example corticosteroids and cyclo-oxygenase inhibitors. However, these drugs have potent and diverse effects and often act by inhibiting events subsequent to initiation of the inflammatory response, leading to more or less severe side-effects, especially when used in high doses for long periods of time. For this reason, strategies aimed at early inhibition of recruitment and activation of leukocytes have been suggested as safer and more specific approaches to reduce inflammation.

    Leukocyte adhesion to activated endothelium is a prerequisite to the following activation and extravasation, and takes place in the initial phase of inflammation. By using a model that allows leukocytes to adhere to tumour necrosis factor (TNF)-activated endothelial cells, thus mimicking aspects of an inflammatory reaction, we found that uridine, 4-thiouridine and isomaltitol could all reduce adhesion. This suggested that they may have anti-inflammatory potential.

    We therefore tried the three substances in a Sephadex-induced lung inflammation model and found that uridine and 4-thiouridine have several anti-inflammatory effects, such as being able to reduce leukocyte accumulation, decrease TNF protein levels and partly inhibit the oedema induced by Sephadex. Isomaltitol turned out to have immunomodulating, rather than anti-inflammatory, effects, which could be of interest in diseases where inadequate inflammatory responses are a problem.

    List of papers
    1. Effects of uridine, isomatitol and 4-thiouridine on in vitro cell adhesion and in vivo effects of 4-thiouridine in a lung inflammation model.
    Open this publication in new window or tab >>Effects of uridine, isomatitol and 4-thiouridine on in vitro cell adhesion and in vivo effects of 4-thiouridine in a lung inflammation model.
    2004 (English)In: International Immunopharmacology, ISSN 1567-5769, E-ISSN 1878-1705, Vol. 4, no 9, p. 1241-1248Article in journal (Refereed) Published
    Abstract [en]

    Since leukocyte adhesion to endothelial cells is crucial for extravasation of leukocytes to sites of inflammation, inhibition of cell-cell adhesion has been suggested as a means to achieve selective modulation of the immune system. We have, using a static in vitro adhesion assay involving adhesion of granulocytes to tumor necrosis factor alpha (TNFalpha)-stimulated human umbilical vein endothelial cells (HUVEC), found three substances--uridine, isomaltitol and 4-thiouridine-that, independently and significantly, reduced leukocyte adhesion by approximately 30-65%. 4-Thiouridine was also tested in an in vivo model of Sephadex (SDX)-induced lung inflammation with Sprague-Dawley rats. Intratracheal instillation of Sephadex (5 mg/kg) alone resulted in a dramatic increase in lung edema and total leukocyte count after 24 h. A differential count of bronchoalveolar lavage (BAL) cells indicated an increased influx of macrophages, eosinophils and neutrophils. Co-administration of 4-thiouridine significantly reduced lung edema by 38%. There was also a significant reduction of the total leukocyte count by 58%. The differential leukocyte count indicated that eosinophil influx alone was reduced by 70%. After Sephadex challenge, we found elevated levels of TNFalpha--an important inflammatory mediator--in the bronchoalveolar lavage fluid (BALF). TNFalpha levels were significantly reduced by more than 80% by co-administration of 4-thoiuridine. These results suggest that uridine, isomaltitol and, especially, 4-thiouridine affect adhesion between leukocytes and activated endothelium, and warrant further in vitro and in vivo studies.

    Keywords
    Inflammation; Adhesion; TNFa; Uridine; Isomaltitol; 4-thiouridine
    National Category
    Medical and Health Sciences
    Identifiers
    urn:nbn:se:liu:diva-19093 (URN)10.1016/j.intimp.2004.04.016 (DOI)15251120 (PubMedID)
    Available from: 2009-06-11 Created: 2009-06-11 Last updated: 2017-12-13Bibliographically approved
    2. 4-Thiouridine induces dose-dependent reduction of oedema, leucocyte influx and tumour necrosis factor in lung inflammation
    Open this publication in new window or tab >>4-Thiouridine induces dose-dependent reduction of oedema, leucocyte influx and tumour necrosis factor in lung inflammation
    2009 (English)In: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 155, no 2, p. 330-338Article in journal (Refereed) Published
    Abstract [en]

    Recent reports demonstrate a role for nucleotides as inflammatory modulators. Uridine, for example, reduces oedema formation and leucocyte infiltration in a Sephadex-induced lung inflammation model. Tumour necrosis factor (TNF) concentration was also reduced. Previous in vivo observations indicated that 4-thiouridine might have similar effects on leucocyte infiltration and TNF release. The aim of this study was thus to investigate the effects of 4-thiouridine in greater detail. We used a Sephadex-induced acute lung inflammation model in Sprague-Dawley rats. The dextran beads were instilled intratracheally into the lungs, which were excised and examined after 24 h. Sephadex alone led to massive oedema formation and infiltration of macrophages, neutrophils and eosinophils. Microgranulomas with giant cell formations were clearly visible around the partially degraded beads. A significant increase in bronchoalveolar lavage fluid (BALF) content of TNF and leukotrienes was also seen. 4-Thiouridine co-administration affected all variables investigated in this model, i.e. oedema, microscopic and macroscopic appearance of lung tissue, total leucocyte and differential leucocyte counts in BALF, TNF and leukotrienes C-4 (LTC4), LTD4 and LTE4 in BALF, indicating a reproducible anti-inflammatory effect. In conclusion, we have demonstrated that 4-thiouridine has anti-inflammatory effects similar to those of uridine. To our knowledge, this is the first demonstration of pharmacological 4-thiouridine effects in vivo. The results suggest nucleoside/nucleotide involvement in inflammatory processes, warranting further studies on nucleoside analogues as attractive new alternatives in the treatment of inflammatory diseases.

    Keywords
    4-thiouridine, inflammation, leukotriene, TNF, uridine
    National Category
    Medical and Health Sciences
    Identifiers
    urn:nbn:se:liu:diva-16418 (URN)10.1111/j.1365-2249.2008.03795.x (DOI)
    Note
    The definitive version is available at www.blackwell-synergy.com: Chamilly Evaldsson, Ingvar Rydén, Anders Rosén and Srinivas Uppugunduri, 4-Thiouridine induces dose-dependent reduction of oedema, leucocyte influx and tumour necrosis factor in lung inflammation, 2009, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, (155), 2, 330-338. http://dx.doi.org/10.1111/j.1365-2249.2008.03795.x Copyright: Blackwell Publishing Ltd http://www.blackwellpublishing.com/ Available from: 2009-01-28 Created: 2009-01-23 Last updated: 2017-12-14Bibliographically approved
    3. Anti-inflammatory effects of exogenous uridine in an animal model of lung inflammation.
    Open this publication in new window or tab >>Anti-inflammatory effects of exogenous uridine in an animal model of lung inflammation.
    2007 (English)In: International Immunopharmacology, ISSN 1567-5769, E-ISSN 1878-1705, Vol. 7, no 8, p. 1025-1032Article in journal (Refereed) Published
    Abstract [en]

    Nucleosides like adenosine, uridine and their nucleotide derivatives (e.g. ATP and UTP) play important roles in many cellular functions, sometimes by acting as signalling molecules through binding to specific P2 nucleotide receptors. P2 receptors are subdivided into P2X and P2Y subfamilies, the latter of which are G-protein coupled receptors. P2Y receptors and nucleoside transporters have been detected in human and rat lungs, where they mediate effects of interest in airway diseases. The aim of this study was to investigate whether uridine has any anti-inflammatory properties in an asthma-like animal model of lung inflammation.

    The Sephadex-induced lung inflammation model in Sprague-Dawley rats was chosen mainly due to its localised inflammatory response and uridine's limited oral bioavailability. The dextran beads, with or without the addition of uridine, were instilled intratracheally into the lungs, which were excised and examined after 24 h.

    Sephadex alone led to massive oedema and infiltration of macrophages, neutrophils and eosinophils. Microgranulomas with giant cell formations were clearly visible around the partially degraded beads. Uridine reduced both the oedema and the infiltration of leukocytes significantly, measured as lung wet weight and leukocyte counts in bronchoalveolar lavage fluid, respectively. Uridine appeared to affect the tumour necrosis factor (TNF) levels, although this could not be statistically confirmed due to large variations within the Sephadex control group.

    We conclude that uridine has anti-inflammatory effects, and that the exact mechanism(s) of action requires further study.

    Keywords
    Asthma, Inflammation, Leukocytes, Sephadex, Tumour necrosis factor, Uridine
    National Category
    Medical and Health Sciences
    Identifiers
    urn:nbn:se:liu:diva-19095 (URN)10.1016/j.intimp.2007.03.008 (DOI)17570319 (PubMedID)
    Available from: 2009-06-11 Created: 2009-06-11 Last updated: 2017-12-13Bibliographically approved
    4. Isomaltitol exacerbates neutrophilia but reduces eosinophilia: New insights into the Sephadex model of lung inflammation
    Open this publication in new window or tab >>Isomaltitol exacerbates neutrophilia but reduces eosinophilia: New insights into the Sephadex model of lung inflammation
    2011 (English)In: International Archives of Allergy and Immunology, ISSN 1018-2438, E-ISSN 1423-0097, Vol. 154, no 4, p. 286-294Article in journal (Refereed) Published
    Abstract [en]

    We have previously examined isomaltitol in an in vitro static adhesion assay between isolated granulocytes and cultured human umbilical cord vein cells and were interested in investigating whether the potentially anti-inflammatory effects observed there could be reproduced in vivo. The Sephadex-induced lung inflammation model was considered a suitable model due to the significant changes in global inflammatory endpoints, like oedema and leukocyte migration, usually seen upon provocation with Sephadex.

    Male Sprague-Dawley rats were instilled intratracheally with Sephadex (5 mg/ml), vehicle (0.9% NaCl), isomaltitol (50 mg/ml) or a combination of isomaltitol and Sephadex. After 24 h, the lungs were weighed to measure oedema and preserved for histology. Bronchoalveolar lavage fluid was used for analysis of tumour necrosis factor, cysteinyl leukotrienes, and differential and total leukocyte counts. In addition, blood differential counts and thymus weights were analysed.

    Contrary to what we expected from in vitro experiments, differential counts showed that isomaltitol increased the neutrophil component while decreasing the eosinophilia. Isomaltitol thus asserted a modulatory role on the usually eosinophil-dominated Sephadex-induced cell profile. Isomaltitol alone also increased several inflammatory parameters, including oedema and cysteinyl leukotrienes, and generally aggravated total inflammation in combination with Sephadex. Although the mechanisms were not investigated in this study, the effects could relate to a combination of isomaltitol's osmotic and structure-specific properties.

    Our results indicate that isomaltitol can modulate the inflammatory response induced by Sephadex instillation in addition to have pro-inflammatory effects on it its own, and may therefore provide new insights into the mechanisms of this widely used animal model. Sugar alcohols similar to isomaltitol have already been used to aid mucus clearance in cystic fibrosis patients, and it is possible that isomaltitol could also be used for this purpose.

    Place, publisher, year, edition, pages
    Karger, 2011
    Keywords
    Isomaltitol, Sephadex, inflammation, oedema, asthma
    National Category
    Respiratory Medicine and Allergy Pharmacology and Toxicology
    Identifiers
    urn:nbn:se:liu:diva-19097 (URN)10.1159/000321820 (DOI)000288529200003 ()
    Note
    Original Publication: Chamilly Evaldsson, Ingvar Rydén and Srinivas Uppugunduri, Isomaltitol exacerbates neutrophilia but reduces eosinophilia: New insights into the Sephadex model of lung inflammation, 2011, International Archives of Allergy and Immunology, (154), 4, 286-294. http://dx.doi.org/10.1159/000321820 Copyright: S. Karger AG http://www.karger.com/ Available from: 2009-06-11 Created: 2009-06-11 Last updated: 2018-01-13Bibliographically approved
  • 9.
    Evaldsson, Chamilly
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Clinical Chemistry. Linköping University, Faculty of Health Sciences.
    Rydén, Ingvar
    Division of Clinical Chemistry, Kalmar County Hospital, Kalmar, Sweden.
    Uppugunduri, Srinivas
    Linköping University, Department of Clinical and Experimental Medicine, Clinical Chemistry. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Diagnostics, Department of Clinical Chemistry.
    Isomaltitol exacerbates neutrophilia but reduces eosinophilia: New insights into the Sephadex model of lung inflammation2011In: International Archives of Allergy and Immunology, ISSN 1018-2438, E-ISSN 1423-0097, Vol. 154, no 4, p. 286-294Article in journal (Refereed)
    Abstract [en]

    We have previously examined isomaltitol in an in vitro static adhesion assay between isolated granulocytes and cultured human umbilical cord vein cells and were interested in investigating whether the potentially anti-inflammatory effects observed there could be reproduced in vivo. The Sephadex-induced lung inflammation model was considered a suitable model due to the significant changes in global inflammatory endpoints, like oedema and leukocyte migration, usually seen upon provocation with Sephadex.

    Male Sprague-Dawley rats were instilled intratracheally with Sephadex (5 mg/ml), vehicle (0.9% NaCl), isomaltitol (50 mg/ml) or a combination of isomaltitol and Sephadex. After 24 h, the lungs were weighed to measure oedema and preserved for histology. Bronchoalveolar lavage fluid was used for analysis of tumour necrosis factor, cysteinyl leukotrienes, and differential and total leukocyte counts. In addition, blood differential counts and thymus weights were analysed.

    Contrary to what we expected from in vitro experiments, differential counts showed that isomaltitol increased the neutrophil component while decreasing the eosinophilia. Isomaltitol thus asserted a modulatory role on the usually eosinophil-dominated Sephadex-induced cell profile. Isomaltitol alone also increased several inflammatory parameters, including oedema and cysteinyl leukotrienes, and generally aggravated total inflammation in combination with Sephadex. Although the mechanisms were not investigated in this study, the effects could relate to a combination of isomaltitol's osmotic and structure-specific properties.

    Our results indicate that isomaltitol can modulate the inflammatory response induced by Sephadex instillation in addition to have pro-inflammatory effects on it its own, and may therefore provide new insights into the mechanisms of this widely used animal model. Sugar alcohols similar to isomaltitol have already been used to aid mucus clearance in cystic fibrosis patients, and it is possible that isomaltitol could also be used for this purpose.

  • 10.
    Gulyas, Miklos
    et al.
    Genetics and Pathology , Uppsala University , Uppsala , Sweden.
    Mattsson, Johanna Sofia Margareta
    Genetics and Pathology , Uppsala University , Uppsala , Sweden.
    Lindgren, Andrea
    Region Östergötland, Heart and Medicine Center, Allergy Center. Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Ek, Lars
    Skane University Hospital , Lund , Sweden.
    Lamberg Lundström, Kristina
    Akademiska Hospital , Uppsala , Sweden.
    Behndig, Annelie
    Norrland University Hospital , Umeå , Sweden.
    Holmberg, Erik
    Sahlgrenska Academy at University of Gothenburg , Sweden.
    Micke, Patrick
    Genetics and Pathology , Uppsala University , Uppsala , Sweden.
    Bergman, Bengt
    Sahlgrenska Academy at University of Gothenburg , Sweden..
    COX-2 expression and effects of celecoxib in addition to standard chemotherapy in advanced non-small cell lung cancer2018In: Acta Oncologica, ISSN 0284-186X, E-ISSN 1651-226X, Vol. 57, no 2, p. 244-250Article in journal (Refereed)
    Abstract [en]

    AIM: Inhibition of cyclooxygenase-2 (COX-2) is proposed as a treatment option in several cancer types. However, in non-small cell lung cancer (NSCLC), phase III trials have failed to demonstrate a benefit of adding COX-2 inhibitors to standard chemotherapy. The aim of this study was to analyze COX-2 expression in tumor and stromal cells as predictive biomarker for COX-2 inhibition.

    METHODS: In a multicenter phase III trial, 316 patients with advanced NSCLC were randomized to receive celecoxib (400 mg b.i.d.) or placebo up to one year in addition to a two-drug platinum-based chemotherapy combination. In a subset of 122 patients, archived tumor tissue was available for immunohistochemical analysis of COX-2 expression in tumor and stromal cells. For each compartment, COX-2 expression was graded as high or low, based on a product score of extension and intensity of positively stained cells.

    RESULTS: An updated analysis of all 316 patients included in the original trial, and of the 122 patients with available tumor tissue, showed no survival differences between the celecoxib and placebo arms (HR 1.01; 95% CI 0.81-1.27 and HR 1.12; 95% CI 0.78-1.61, respectively). High COX-2 scores in tumor (n = 71) or stromal cells (n = 55) was not associated with a superior survival outcome with celecoxib vs. placebo (HR =0.96, 95% CI 0.60-1.54; and HR =1.51; 95% CI 0.86-2.66), and no significant interaction effect between COX-2 score in tumor or stromal cells and celecoxib effect on survival was detected (p = .48 and .25, respectively).

    CONCLUSIONS: In this subgroup analysis of patients with advanced NSCLC treated within the context of a randomized trial, we could not detect any interaction effect of COX-2 expression in tumor or stromal cells and the outcome of celecoxib treatment in addition to standard chemotherapy.

  • 11.
    Hellberg, Sandra
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Bhai Mehta, Ratnesh
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Forsberg, Anna
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Berg, Göran
    Linköping University, Department of Clinical and Experimental Medicine, Division of Children's and Women's health. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Gynaecology and Obstetrics in Linköping.
    Brynhildsen, Jan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Children's and Women's health. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Gynaecology and Obstetrics in Linköping.
    Winqvist, Ola
    Karolinska Inst, Sweden.
    Jenmalm, Maria
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Ernerudh, Jan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Immunology and Transfusion Medicine.
    Maintained thymic output of conventional and regulatory T cells during human pregnancy2019In: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 143, no 2, p. 771-775.e7Article in journal (Other academic)
    Abstract [en]

    n/a

  • 12.
    Hjalmarsson, Clara
    et al.
    Sahlgrens Univ Hosp, Sweden; Gothenburg Univ, Sweden.
    Radegran, Goran
    Skane Univ Hosp, Sweden; Lund Univ, Sweden.
    Kylhammar, David
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Clinical Physiology in Linköping.
    Rundqvist, Bengt
    Sahlgrens Univ Hosp, Sweden; Gothenburg Univ, Sweden.
    Multing, Jonas
    Sahlgrens Univ Hosp, Sweden; Gothenburg Univ, Sweden.
    Nisell, Magnus D.
    Karolinska Inst, Sweden.
    Kjellstrom, Barbro
    Karolinska Inst, Sweden.
    Impact of age and comorbidity on risk stratification in idiopathic pulmonary arterial hypertension2018In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 51, no 5, article id 1702310Article in journal (Refereed)
    Abstract [en]

    Recent reports from worldwide pulmonary hypertension registries show a new demographic picture for patients with idiopathic pulmonary arterial hypertension (IPAH), with an increasing prevalence among the elderly. We aimed to investigate the effects of age and comorbidity on risk stratification and outcome of patients with incident IPAH. The study population (n=264) was categorised into four age groups: 18-45, 46-64, 65-74 and amp;gt;= 75 years. Individual risk profiles were determined according to a risk assessment instrument, based on the European Society of Cardiology and the European Respiratory Society guidelines. The change in risk group from baseline to follow-up (median 5 months) and survival were compared across age groups. In the two youngest age groups, a significant number of patients improved (18-45 years, Z=-4.613, pamp;lt; 0.001; 46-64 years, Z=-2.125, p=0.034), but no significant improvement was found in the older patient groups. 5-year survival was highest in patients aged 18-45 years (88%), while the survival rates were 63%, 56% and 36% for patients in the groups 46-64, 65-74 and. 75 years, respectively (pamp;lt; 0.001). Ischaemic heart disease and kidney dysfunction independently predicted survival. These findings highlight the importance of age and specific comorbidities as prognostic markers of outcome in addition to established risk assessment algorithms.

  • 13.
    Kentson, Magnus
    et al.
    Linköping University, Department of Medical and Health Sciences. Linköping University, Faculty of Medicine and Health Sciences. Division of Medicine, Ryhov Hospital, Jönköping, Sweden.
    Leanderson, Per
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center.
    Jacobson, Petra
    Linköping University, Department of Medical and Health Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    Persson, Hans Lennart
    Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine. Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine.
    Oxidant status, iron homeostasis, and carotenoid levels of COPD patients with advanced disease and LTOT2018In: European Clinical Respiratory Journal, ISSN 2001-8525, Vol. 5, no 1Article in journal (Refereed)
    Abstract [en]

    Background: The pathogenesis of chronic obstructive pulmonary disease (COPD) is associated with oxidative stress. Both iron (Fe) and oxygen are involved in the chemical reactions that lead to increased formation of reactive oxygen species. Oxidative reactions are prevented by antioxidants such as carotenoids. Objective: To study the differences in Fe status, carotenoid levels, healthy eating habits, and markers of inflammation and oxidative damage on proteins in subjects with severe COPD ± long-term oxygen therapy (LTOT) and lung-healthy control subjects. Methods: Sixty-six Caucasians with advanced COPD (28 with LTOT) and 47 control subjects were included. Questionnaires about general health, lifestyle, and dietary habits were answered. Lung function tests and blood sampling were performed. Results: COPD subjects (±LTOT) did not demonstrate increased oxidative damage, assessed by protein carbonylation (PC), while levels of soluble transferrin receptors (sTfRs) were slightly elevated. Soluble TfRs, which is inversely related to Fe status, was negatively associated with PC. Levels of carotenoids, total and ß-cryptoxanthin, a- and ß-carotenes, were significantly lower in COPD subjects, and their diet contained significantly less fruits and vegetables. Lutein correlated inversely with IL-6, lycopene correlated inversely with SAT, while ß-carotene was positively associated with a Mediterranean-like diet. Conclusions: Fe could favor oxidative stress in COPD patients, suggesting a cautious use of Fe prescription to these patients. COPD subjects ate a less healthy diet than control subjects did and would, therefore, benefit by dietary counseling. COPD patients with hypoxemia are probably in particular need of a lycopene-enriched diet.

  • 14.
    Kentson, Magnus
    et al.
    Linköping University, Department of Medical and Health Sciences. Linköping University, Faculty of Medicine and Health Sciences. Division of Medicine, Ryhov Hospital, Jönköping, Sweden.
    Leandersson, Per
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center.
    Jacobson, Petra
    Linköping University, Department of Medical and Health Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    Persson, Lennart
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    The influence of disease severity and lifestyle factors on the peak annual 25(OH)D value of COPD patients2018In: The International Journal of Chronic Obstructive Pulmonary Disease, ISSN 1176-9106, E-ISSN 1178-2005, Vol. 13, p. 1389-1398Article in journal (Refereed)
    Abstract [en]

    Background: The prevalence of individuals deficient in vitamin D (defined as a serum level of the stable metabolite 25(OH)D amp;lt; 50 nmol/L) is increasing in countries with low annual ultraviolet (UV) radiation and among individuals unable to perform outdoor activities, for example, COPD patients. Objective: To assess the role of vitamin D deficiency, independently of seasonal variation, the peak annual value of 25(OH)D was measured in subjects with advanced COPD +/- long-term oxygen therapy (LTOT) and lung healthy control subjects. A method to grade the individual annual UV light exposure was designed and tested. Subjects and methods: Sixty-six Caucasians with advanced COPD (28 with LTOT) and 47 control subjects were included, and the levels of 25(OH)D were determined in late summer/ early fall when the annual peak was assumed. Questionnaires about COPD symptoms, general health, lifestyle, dietary habits and QoL were used to collect data. Lung function tests and blood sampling were performed. Results: The peak annual 25(OH)D of COPD subjects was significantly lower than in the control subjects, but there was no significant difference between COPD patients with and without LTOT. Ongoing vitamin D supplementation was the single most important intervention to maintain 25(OH)D levels amp;gt;= 50 nmol/L. Among vitamin D-deficient COPD subjects, 25(OH)D correlated positively with forced expiratory volume in 1 second as % predicted, Modified British Medical Research Council score, blood oxygenation, food portion size, Mediterranean Diet Score and Ultraviolet Score. Conclusion: Vitamin D deficiency was common among healthy individuals and COPD subjects. Peak annual 25(OH)D levels of COPD subjects correlated with clinically important outcomes. The present study emphasizes the need to routinely monitor vitamin D status among patients with advanced COPD and to consider to medicate those with vitamin D deficiency with vitamin D supplementation.

  • 15.
    Kentson, Magnus
    et al.
    Linköping University, Department of Medical and Health Sciences. Linköping University, Faculty of Medicine and Health Sciences. Ryhov County Hospital, Sweden.
    Tödt, Kristina
    Linköping University, Faculty of Medicine and Health Sciences. Linköping University, Department of Medical and Health Sciences, Division of Physiotherapy. Skåne University Hospital, Sweden.
    Skargren, Elisabeth
    Linköping University, Faculty of Medicine and Health Sciences. Linköping University, Department of Medical and Health Sciences.
    Jakobsson, Per
    Ryhov County Hospital, Sweden.
    Ernerudh, Jan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Immunology and Transfusion Medicine.
    Unosson, Mitra
    Linköping University, Department of Social and Welfare Studies, Division of Nursing Science. Linköping University, Faculty of Medicine and Health Sciences.
    Theander, Kersti
    Karlstad University, Sweden; County Council Varmland, Sweden.
    Factors associated with experience of fatigue, and functional limitations due to fatigue in patients with stable COPD2016In: THERAPEUTIC ADVANCES IN RESPIRATORY DISEASE, ISSN 1753-4658, Vol. 10, no 5, p. 410-424Article in journal (Refereed)
    Abstract [en]

    Background: The aim of this study was to determine the influence of selected physiological, psychological and situational factors on experience of fatigue, and functional limitations due to fatigue in patients with stable chronic obstructive pulmonary disease (COPD). Methods: In total 101 patients with COPD and 34 control patients were assessed for experience of fatigue, functional limitation due to fatigue (Fatigue Impact Scale), physiological [lung function, 6-minute walk distance (6MWD), body mass index (BMI), dyspnoea, interleukin (IL)-6, IL-8, high sensitivity C-reactive protein (hs-CRP), surfactant protein D], psychological (anxiety, depression, insomnia), situational variables (age, sex, smoking, living alone, education), and quality of life. Results: Fatigue was more common in patients with COPD than in control patients (72% versus 56%, p amp;lt; 0.001). Patients with COPD and fatigue had lower lung function, shorter 6MWD, more dyspnoea, anxiety and depressive symptoms, and worse health status compared with patients without fatigue (all p amp;lt; 0.01). No differences were found for markers of systemic inflammation. In logistic regression, experience of fatigue was associated with depression [odds ratio (OR) 1.69, 95% confidence interval (CI) 1.28-2.25) and insomnia (OR 1.75, 95% CI 1.19-2.54). In linear regression models, depression, surfactant protein D and dyspnoea explained 35% (R-2) of the variation in physical impact of fatigue. Current smoking and depression explained 33% (R-2) of the cognitive impact of fatigue. Depression and surfactant protein D explained 48% (R-2) of the psychosocial impact of fatigue. Conclusions: Experiences of fatigue and functional limitation due to fatigue seem to be related mainly to psychological but also to physiological influencing factors, with depressive symptoms, insomnia problems and dyspnoea as the most prominent factors. Systemic inflammation was not associated with perception of fatigue but surfactant protein D was connected to some dimensions of the impact of fatigue

  • 16.
    Kylhammar, David
    et al.
    Region Östergötland, Heart and Medicine Center, Department of Clinical Physiology in Linköping.
    Rådegran, Göran
    Sektionen för Hjärtsvikt och klaffsjukdomar, Hjärt- och lungkliniken SUS Lund, Sweden.
    Pulmonell hypertension vanligt vid kronisk lungsjukdom - Europeiska riktlinjer kring utredning och behandling2017In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 114Article, review/survey (Refereed)
    Abstract [en]

    Pulmonary hypertension due to lung diseases In 2015 the European Society of Cardiology and European Respiratory Society published new guidelines on the diagnosis and treatment of pulmonary hypertension (PH). PH due to lung diseases and/or hypoxia was classified as a separate entity. PH is common in lung diseases, but seldom severe. Nevertheless, the presence of PH in a patient with lung disease is associated with worse outcome. If there is clinical suspicion of PH in a patient with lung disease, echocardiography is recommended, and if there are signs of severe PH and/or severe right ventricular dysfunction the patient should be referred to a PH expert centre. Patients may have lung disease and e.g. pulmonary arterial hypertension or chronic thromboembolic PH simultaneously, and targeted treatments are available in such cases. PH-targeted drugs should, however, not be used to treat PH due to lung diseases, since there are no robust data speaking for their benefit and a risk of impaired arterial oxygenation due to inhibition of hypoxic pulmonary vasoconstriction. Instead, the underlying lung disease should be optimally treated, including long-term oxygen therapy in case of chronic hypoxemia.

  • 17.
    Lange, C.
    et al.
    Res Ctr Borstel, Germany; Univ Lubeck, Germany; German Ctr Infect Res DZIF, Germany; Karolinska Inst, Sweden.
    Aarnoutse, R. E.
    Radboud Univ Nijmegen, Netherlands.
    Alffenaar, J. W. C.
    Univ Groningen, Netherlands.
    Bothamley, G.
    Homerton Univ Hosp, England; QMUL, England; London Sch Hyg and Trop Med, England.
    Brinkmann, F.
    Ruhr Univ Bochum, Germany.
    Costa, J.
    Ctr Hosp Leiria, Portugal; Ctr Innovat Technol and Hlth Care, Portugal.
    Chesov, D.
    Nicoale Testemitanu State Univ Med and Pharm, Moldova; Res Ctr Borstel, Germany.
    van Crevel, R.
    Radboud Univ Nijmegen, Netherlands; Univ Oxford, England.
    Dedicoat, M.
    Univ Hosp Birmingham, England.
    Dominguez, J.
    Univ Autonoma Barcelona, Spain.
    Duarte, R.
    Portuguese Natl TB Program, Portugal; Ctr Hosp Vila Nova de Gaia, Portugal; Univ Porto, Portugal; Univ Porto, Portugal.
    Grobbel, H. P.
    Res Ctr Borstel, Germany; Univ Lubeck, Germany; German Ctr Infect Res DZIF, Germany.
    Guenther, G.
    Res Ctr Borstel, Germany; Univ Namibia, Namibia.
    Guglielmetti, L.
    Hop Univ Pitie Salpetriere Charles Foix, France; Univ Pierre and Marie Curie 06, France.
    Heyckendorf, J.
    Res Ctr Borstel, Germany; Univ Lubeck, Germany; German Ctr Infect Res DZIF, Germany.
    Kay, A. W.
    Texas Childrens Hosp, TX 77030 USA; Baylor Coll Med, TX 77030 USA; Baylor Coll Med Childrens Fdn, Swaziland.
    Kirakosyan, O.
    MSF France OCP, Armenia.
    Kirk, O.
    Univ Copenhagen, Denmark; Univ Southern Denmark, Denmark.
    Koczulla, R. A.
    Philipps Univ Marburg, Germany; German Ctr Lung Res DZL, Germany.
    Kudriashov, G. G.
    St Petersburg State Res Inst Phthisiopulmonol, Russia.
    Kuksa, L.
    Riga East Univ Hosp, Latvia; Riga Stradins Univ, Latvia.
    van Leth, F.
    Univ Amsterdam, Netherlands.
    Magis-Escurra, C.
    Radboud Univ Nijmegen, Netherlands.
    Mandalakas, A. M.
    Texas Childrens Hosp, TX 77030 USA; Baylor Coll Med, TX 77030 USA.
    Molina-Moya, B.
    Univ Autonoma Barcelona, Spain.
    Peloquin, C. A.
    Univ Florida, FL USA.
    Reimann, M.
    Res Ctr Borstel, Germany; Univ Lubeck, Germany; German Ctr Infect Res DZIF, Germany.
    Rumetshofer, R.
    Otto Wagner Hosp Vienna, Austria.
    Schaaf, H. S.
    Stellenbosch Univ, South Africa.
    Schön, Thomas
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology, Infection and Inflammation. Linköping University, Faculty of Medicine and Health Sciences. Kalmar Cty Hosp, Sweden.
    Tiberi, S.
    Barts Hlth NHS Trust, England; Queen Mary Univ, England.
    Valda, J.
    Otto Wagner Hosp Vienna, Austria.
    Yablonskii, P. K.
    St Petersburg State Res Inst Phthisiopulmonol, Russia; St Petersburg State Univ, Russia.
    Dheda, K.
    Univ Cape Town, South Africa.
    Management of patients with multidrug-resistant tuberculosis2019In: The International Journal of Tuberculosis and Lung Disease, ISSN 1027-3719, E-ISSN 1815-7920, Vol. 23, no 6, p. 645-662Article in journal (Refereed)
    Abstract [en]

    The emergence of multidrug-resistant tuberculosis (MDR-TB; defined as resistance to at least rifampicin and isoniazid) represents a growing threat to public health and economic growth. Never before in the history of mankind have more patients been affected by MDR-TB than is the case today. The World Health Organization reports that MDR-TB outcomes are poor despite staggeringly high management costs. Moreover, treatment is prolonged, adverse events are common, and the majority of affected patients do not receive adequate treatment. As MDR-TB strains are often resistant to one or more second-line anti-TB drugs, in-depth genotypic and phenotypic drug susceptibility testing is needed to construct personalised treatment regimens to improve treatment outcomes. For the first time in decades, the availability of novel drugs such as bedaquiline allow us to design potent and well-tolerated personalised MDR-TB treatment regimens based solely on oral drugs. In this article, we present management guidance to optimise the diagnosis, algorithm-based treatment, drug dosing and therapeutic drug monitoring, and the management of adverse events and comorbidities, associated with MDR-TB. We also discuss the role of surgery, physiotherapy, rehabilitation, palliative care and smoking cessation in patients with MDR-TB. We hope that incorporating these recommendations into patient care will be helpful in optimising treatment outcomes, and lead to more MDR-TB patients achieving a relapse-free cure.

  • 18.
    Lind, Leili
    et al.
    Linköping University, Department of Biomedical Engineering, Division of Biomedical Engineering. Linköping University, Faculty of Science & Engineering.
    Lyth, Johan
    Region Östergötland, Regional Board, Research and Development Unit.
    Karlsson, Daniel M. G.
    Linköping University, Department of Biomedical Engineering.
    Wiréhn, Ann-Britt
    Region Östergötland, Regional Board, Research and Development Unit.
    Persson, Lennart
    Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    COPD patients require more health care than heart failure patients2018In: ERS International Congress 2018, 2018Conference paper (Refereed)
    Abstract [en]

    Background: Populations of elderly patients with advanced stages of chronic obstructive pulmonary disease (COPD) or heart failure (HF) are growing, urging the need for specialized health care in the patients’ home. A 4 year (2013-2017) telehealth intervention single-centre clinical study has been completed. We hypothesized that the two groups of patients, advanced COPD or HF, would exhibit differences regarding exacerbations and the need of health care.

    Objective: To study exacerbations of COPD or HF, and patients’ need of health care.

    Methods: A telemonitoring system, the Health Diary, which is based on digital pen technology, was employed. Patients with at least 2 hospital admissions the previous year were included. Responsible nurses and physicians at a specialized home care unit at a university hospital checked all daily patient reports. Physicians identified exacerbations using information provided through the telemonitoring system and patient contacts. Consumed health care was assessed as the number of patient contacts (home visits or telephone consultations).

    Results: Totally, 94 patients with advanced disease were enrolled (36 COPD and 58 HF patients) of which 53 patients (19 COPD and 34 HF patients) completed the 1-yr study period. The major reason for not completing the study was death (13 COPD, 15 HF patients). Average numbers of exacerbations were 3.1 and 0.8 and patient contacts were 94 and 67 per COPD and HF patient, respectively.

    Conclusions: Compared to HF patients, COPD patients exhibit exacerbations more frequently and demand much more home health care. This difference of health care consumption is mainly due to disease characteristics.

  • 19.
    Lyth, Johan
    et al.
    Region Östergötland, Regional Board, Research and Development Unit.
    Lind, Leili
    Linköping University, Department of Biomedical Engineering, Division of Biomedical Engineering. Linköping University, Faculty of Science & Engineering.
    Karlsson, Daniel
    The National Board of Health and Welfare, Department for Knowledge-Based Policy of Social Services, eHealth and Structured Information Unit, Stockholm, Sweden.
    Persson, Lennart Hans
    Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    Wiréhn, Ann-Britt
    Region Östergötland, Regional Board, Research and Development Unit.
    Can a telemonitoring system lead to decreased hospital admissions in elderly patients?2018Conference paper (Refereed)
    Abstract [en]

    Background: Populations of elderly patients with chronic obstructive pulmonary disease (COPD) or heart failure (HF) are growing. To prevent exacerbations leading to inpatient care, a 4 year (2013-2017) telehealth intervention non-randomized single-centre clinical study was performed. We hypothesized that the patients, grouped by advanced COPD or HF, would exhibit decreased need of hospital admissions.

    Objective: To study hospital admissions in patients with COPD or HF using a telemonitoring system, the Health Diary.

    Methods: A telemonitoring system, the Health Diary, based on digital pen technology, was employed. Patients with COPD or HF treated at the University Hospital in Linköping were included if they had at least 2 hospital admissions the previous year. Data on hospital admissions was obtained from the administrative healthcare database. Expected number of hospital admissions for the study year was calculated using 5-year data for a group of patients with matching diagnosis and history of hospital admissions and was compared to the actual value in the intervention group using Poisson regression.

    Results: Together with the included patients, 159 HF and 136 COPD non-intervention patients was used to calculate the expected values for hospital admissions. For the 58 included HF patients, the average number of hospital admissions of 0.81 was 32.8 percent (p=0.04) lower than expected. For the 36 included COPD patients, the average number of hospital admissions of 1.44 was 37.0 percent (p=0.02) lower than expected.

    Conclusions: Use of the telemonitoring system, the Health Diary, decreases hospital admissions in elderly with COPD and HF.

  • 20.
    Løkke, Anders
    et al.
    Department of Respiratory Medicine, Aarhus County Hospital, Aarhus, Denmark.
    Ahlbeck, Lars
    Region Östergötland, Heart and Medicine Center, Allergy Center. Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Respiratory System Drug Committee at Region Östergötland, Linköping, Sweden.
    Bjermer, Leif
    Department of Respiratory Medicine and Allergology, Institute of Clinical Science, Lund University, Lund, Sweden.
    Mortensen, Jann
    Department of Clinical Physiology, Nuclear Medicine and PET, Rigshospitalet, Denmark;Department of Medicine, National Hospital, Torshavn, Faroe Islands.
    Østrem, Anders
    Gransdalen Health Care Centre, Oslo, Norway.
    Pasternack, Iris
    Summaryx Ltd, HTA Research, Helsinki, Finland.
    Safioti, Guilherme
    TEVA Pharmaceuticals, Helsingborg, Sweden.
    Torvinen, Saku
    TEVA Pharmaceuticals BV, Amsterdam, the Netherlands.
    Expert Nordic perspectives on the potential of novel inhalers to overcome unmet needs in the management of obstructive lung disease2015In: European clinical respiratory journal, ISSN 2001-8525, Vol. 2, p. 1-8, article id 29445Article, review/survey (Refereed)
    Abstract [en]

    The effective self-management of obstructive lung disease is dependent upon the patient achieving good inhaler technique. However, many current inhalers are complicated to use, which may lead to handling difficulties. These difficulties can cause clinically relevant errors, whereby pharmacotherapy fails to achieve adequate lung deposition and therapeutic effect. In this report, the potential of novel inhaler devices to overcome unmet needs in the management of obstructive lung disease is considered by a panel of Nordic experts. The panel concludes that innovative inhalers can contribute to good disease management and better use of healthcare resources.

  • 21.
    Menditto, E.
    et al.
    CIRFF, Center of Pharmacoeconomics, University of Naples Federico II, Naples, Italy; University of Naples Federico II, Naples, Italy.
    Costa, E.
    UCIBIO, REQUIMTE, Faculty of Pharmacy, and Competence Center on Active and Healthy Ageing of University of Porto (Porto4Ageing), University of Porto, Porto, Portugal.
    Midão, L.
    UCIBIO, REQUIMTE, Faculty of Pharmacy, and Competence Center on Active and Healthy Ageing of University of Porto (Porto4Ageing), University of Porto, Porto, Portugal.
    Bosnic-Anticevich, S.
    Woolcock Institute of Medical Research, University of Sydney Woolcock Emphysema Centre and Sydney Local Health District, Glebe, NSW, Australia.
    Novellino, E.
    University of Naples Federico II, Naples, Italy.
    Bialek, S.
    Department of Biochemistry and Clinical Chemistry, Faculty of Pharmacy with the Division of Laboratory Medicine, Warsaw Medical University, Warsaw, Poland.
    Briedis, V.
    Lithuanian University of Health Sciences, Kaunas, Lithuania.
    Mair, A.
    DG for Health and Social Care, Scottish Government, Edinburgh, United Kingdom.
    Rajabian-Soderlund, R.
    Department of Nephrology and Endocrinology, Karolinska University Hospital, Stockholm, Sweden.
    Arnavielhe, S.
    KYomed INNOV, Montpellier, France.
    Bedbrook, A.
    MACVIA-France, Fondation partenariale FMC VIA-LR, Montpellier, France.
    Czarlewski, W.
    Medical Consulting Czarlewski, Levallois, France.
    Annesi-Maesano, I.
    Epidemiology of Allergic and Respiratory Diseases, Department Institute Pierre Louis of Epidemiology and Public Health, INSERM and Sorbonne Université, Medical School Saint Antoine, Paris, France.
    Anto, J.M.
    ISGlobAL, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; IMIM (Hospital del Mar Research Institute), Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain.
    Devillier, P.
    Laboratoire de Pharmacologie Respiratoire UPRES EA220, Hôpital Foch, Suresnes, France; Université Versailles Saint-Quentin, Université Paris Saclay, Paris Saclay, France.
    De, Vries G.
    Peercode BV, Geldermalsen, Netherlands.
    Keil, T.
    Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Berlin, Germany; Institute for Clinical Epidemiology and Biometry, University of Wuerzburg, Wuerzburg, Germany.
    Sheikh, A.
    The Usher Institute of Population Health Sciences and Informatics, The University of Edinburgh, Edinburgh, United Kingdom.
    Orlando, V.
    CIRFF, Center of Pharmacoeconomics, University of Naples Federico II, Naples, Italy; University of Naples Federico II, Naples, Italy.
    Larenas-Linnemann, D.
    Center of Excellence in Asthma and Allergy, Médica Sur Clinical Foundation and Hospital, México City, Mexico.
    Cecchi, L.
    SOS Allergology and Clinical Immunology, USL Toscana Centro, Prato, Italy.
    De, Feo G.
    Department of Medicine, Surgery and Dentistry “Scuola Medica Salernitana”, University of Salerno, Salerno, Italy.
    Illario, M.
    Division for Health Innovation, Campania Region and Federico II University Hospital Naples (RandD and DISMET), Naples, Italy.
    Stellato, C.
    Department of Medicine, Surgery and Dentistry “Scuola Medica Salernitana”, University of Salerno, Salerno, Italy.
    Fonseca, J.
    CINTESIS, Center for Research in Health Technologies and Information Systems, Faculdade de Medicina da Universidade do Porto, Porto, Portugal; MEDIDA, Lda, Porto, Portugal.
    Malva, J.
    Faculty of Medicine, Coimbra Institute for Clinical and Biomedical Research (iCBR), University of Coimbra, Coimbra, Portugal; Ageing@Coimbra EIP-AHA Reference Site, Coimbra, Portugal.
    Morais-Almeida, M.
    Allergy Center, CUF Descobertas Hospital, Lisbon, Portugal.
    Pereira, A.M.
    Allergy Unit, CUF-Porto Hospital and Institute, Porto, Portugal; Center for Research in Health Technologies and Information Systems CINTESIS, Universidade do Porto, Porto, Portugal.
    Todo-Bom, A.M.
    Imunoalergologia, Centro Hospitalar Universitário de Coimbra and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
    Kvedariene, V.
    Faculty of Medicine, Vilnius University, Vilnius, Lithuania.
    Valiulis, A.
    Department of Public Health, Clinic of Childrens Diseases, and Institute of Health Sciences, Vilnius University Institute of Clinical Medicine, Vilnius, Lithuania; European Academy of Paediatrics (EAP/UEMS-SP), Brussels, Belgium.
    Bergmann, K.C.
    Charité – Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, Berlin, Germany; Department of Dermatology and Allergy, Comprehensive Allergy Center, Berlin Institute of Health, Berlin, Germany.
    Klimek, L.
    Euforea, Brussels, Belgium.
    Mösges, R.
    Medical Faculty, Institute of Medical Statistics, and Computational Biology, University of Cologne, Cologne, Germany; CRI-Clinical Research International-Ltd, Hamburg, Germany.
    Pfaar, O.
    Department of Otorhinolaryngology, Head and Neck Surgery, Section of Rhinology and Allergy, University Hospital Marburg, Phillipps-Universität Marburg, Germany.
    Zuberbier, T.
    Charité – Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, Berlin, Germany; Department of Dermatology and Allergy, Comprehensive Allergy Center, Berlin Institute of Health, Berlin, Germany.
    Cardona, V.
    Allergy Section, Department of Internal Medicine, Hospital Vall dHebron, and ARADyAL Spanish Research Network, Barcelona, Spain.
    Mullol, J.
    Rhinology Unit and Smell Clinic, ENT Department, Hospital Clínic, Barcelona, Spain; Clinical and Experimental Respiratory Immunoallergy, IDIBAPS, CIBERES, University of Barcelona, Barcelona, Spain.
    Papadopoulos, N.G.
    Division of Infection, Immunityand Respiratory Medicine, Royal Manchester Childrens Hospital, University of Manchester, Manchester, United Kingdom; Allergy Department, 2nd Pediatric Clinic, Athens General Childrens Hospital “PandA Kyriakou”, University of Athens, Athens, Greece.
    Prokopakis, E.P.
    Department of Otorhinolaryngology, University of Crete School of Medicine, Heraklion, Greece.
    Bewick, M.
    iQ4U Consultants Ltd, London, United Kingdom.
    Ryan, D.
    Allergy and Respiratory Research Group, The University of Edinburgh, Edinburgh, United Kingdom.
    Roller-Wirnsberger, R.E.
    Department of Internal Medicine, Medical University of Graz, Graz, Austria.
    Tomazic, P.V.
    Department of ENT, Medical University of Graz, Graz, Austria.
    Cruz, A.A.
    ProAR – Nucleo de Excelencia em Asma, Federal University of Bahia, Salvador, Brazil; WHO GARD Planning Group, Salvador, Brazil.
    Kuna, P.
    Division of Internal Medicine, Asthma and Allergy, Barlicki University Hospital, Medical University of Lodz, Lodz, Poland.
    Samolinski, B.
    Department of Prevention of Envinronmental Hazards and Allergology, Medical University of Warsaw, Warsaw, Poland.
    Fokkens, W.J.
    Department of Otorhinolaryngology, Academic Medical Centre, Amsterdam, Netherlands.
    Reitsma, S.
    Department of Otorhinolaryngology, Academic Medical Centre, Amsterdam, Netherlands.
    Bosse, I.
    Allergist, La Rochelle, France.
    Fontaine, J.-F.
    Allergist, Reims, France.
    Laune, D.
    KYomed INNOV, Montpellier, France.
    Haahtela, T.
    Skin and Allergy Hospital, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
    Toppila-Salmi, S.
    Skin and Allergy Hospital, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
    Bachert, C.
    Upper Airways Research Laboratory, ENT Department, Ghent University Hospital, Ghent, Belgium.
    Hellings, P.W.
    Euforea, Brussels, Belgium.
    Melén, E.
    Sachs’ Children and Youth Hospital, Södersjukhuset, Stockholm, Sweden; Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Wickman, M.
    Centre for Clinical Research Sörmland, Uppsala University, Eskilstuna, Sweden.
    Bindslev-Jensen, C.
    Department of Dermatology and Allergy Centre, Odense University Hospital, Odense Research Center for Anaphylaxis (ORCA), Odense, Denmark.
    Eller, E.
    Department of Dermatology and Allergy Centre, Odense University Hospital, Odense Research Center for Anaphylaxis (ORCA), Odense, Denmark.
    OHehir, R.E.
    Department of Allergy, Immunology and Respiratory Medicine, Alfred Hospital and Central Clinical School, Monash University, Melbourne, VIC, Australia; Department of Immunology, Monash University, Melbourne, VIC, Australia.
    Cingi, C.
    ENT Department, Medical Faculty, Eskisehir Osmangazi University, Eskisehir, Turkey.
    Gemicioglu, B.
    Department of Pulmonary Diseases, Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey.
    Kalayci, O.
    Pediatric Allergy and Asthma Unit, Hacettepe University School of Medicine, Ankara, Turkey.
    Ivancevich, J.C.
    Servicio de Alergia e Immunologia, Clinica Santa Isabel, Buenos Aires, Argentina.
    Bousquet, J.
    Euforea, Brussels, Belgium.
    the, MASK group
    Adherence to treatment in allergic rhinitis using mobile technology. The MASK Study2019In: Clinical and Experimental Allergy, ISSN 0954-7894, E-ISSN 1365-2222, Vol. 49, no 4, p. 442-460Article in journal (Refereed)
    Abstract [en]

    Background

    Mobile technology may help to better understand the adherence to treatment. MASK‐rhinitis (Mobile Airways Sentinel NetworK for allergic rhinitis) is a patient‐centred ICT system. A mobile phone app (the Allergy Diary) central to MASK is available in 22 countries.

    Objectives

    To assess the adherence to treatment in allergic rhinitis patients using the Allergy DiaryApp.

    Methods

    An observational cross‐sectional study was carried out on all users who filled in the Allergy Diary from 1 January 2016 to 1 August 2017. Secondary adherence was assessed by using the modified Medication Possession Ratio (MPR) and the Proportion of days covered (PDC) approach.

    Results

    A total of 12 143 users were registered. A total of 6 949 users reported at least one VAS data recording. Among them, 1 887 users reported ≥7 VAS data. About 1 195 subjects were included in the analysis of adherence. One hundred and thirty‐six (11.28%) users were adherent (MPR ≥70% and PDC ≤1.25), 51 (4.23%) were partly adherent (MPR ≥70% and PDC = 1.50) and 176 (14.60%) were switchers. On the other hand, 832 (69.05%) users were non‐adherent to medications (MPR <70%). Of those, the largest group was non‐adherent to medications and the time interval was increased in 442 (36.68%) users.

    Conclusion and clinical relevance

    Adherence to treatment is low. The relative efficacy of continuous vs on‐demand treatment for allergic rhinitis symptoms is still a matter of debate. This study shows an approach for measuring retrospective adherence based on a mobile app. This also represents a novel approach for analysing medication‐taking behaviour in a real‐world setting.

  • 22.
    Naidu Sjöswärd, Kerstin
    et al.
    Linköping University, Department of Medicine and Care. Linköping University, Faculty of Health Sciences.
    Uppugunduri, Srinivas
    Linköping University, Department of Medicine and Care. Linköping University, Faculty of Health Sciences.
    Schmekel, Birgitta
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Decreased serum levels of P-selectin and eosinophil cationic protein in patients with mild asthma after inhaled salbutamol2004In: Respiration, ISSN 0025-7931, E-ISSN 1423-0356, Vol. 71, no 3, p. 241-245Article in journal (Refereed)
    Abstract [en]

    Background: Asthma is a chronic inflammatory disease of the airways associated with selective recruitment of activated eosinophils. P-selectin, a cell adhesion molecule, may be an important controller of the inflammation by mediating selective eosinophil cell influx to the lung. Serum levels of eosinophil cationic protein (ECP) have been used as a marker of eosinophil inflammation, and indirectly as a marker of disease activity of asthma. ECP levels may not be elevated in some patients with asthma, and this fact prompted us to search for additional surrogate markers for monitoring disease activity in asthma. Objectives: To evaluate whether repeated inhalations of salbutamol, a ß-2-receptor agonist used for bronchodilation, would lead to reduced serum levels of P-selectin and/or ECP. Methods: Fourteen patients with asymptomatic mild stable asthma were enrolled into a randomised crossover study. Salbutamol was inhaled three times every 3 h. Blood was sampled 4 h after the last inhalation. Nine non-treated healthy volunteers served as control subjects. Serum ECP and P-selectin levels were measured using radioimmunoassay and ELISA, respectively. Results: P-selectin and ECP levels in serum obtained from asymptomatic asthmatics were close to those of the volunteers, and inter-day variability tended to be lower for levels of P-selectin than for ECP. Significant decreases of P-selectin (p = 0.01) and ECP (p = 0.03) were recorded after salbutamol inhalation. There was no association between the changes in ECP and P-selectin levels in serum. Conclusions: We conclude that decreases in P-selectin and ECP may have different kinetics, suggesting different pathways of action of salbutamol. We judge that P-selectin may be used as a sensitive marker in mild asthma. Copyright © 2004 S. Karger AG, Basel.

  • 23.
    Nilsson, A. M.
    et al.
    Region Östergötland, Heart and Medicine Center, Department of Rheumatology. Lund Univ, Sweden.
    Tufvesson, E.
    Lund Univ, Sweden.
    Hesselstrand, R.
    Lund Univ, Sweden.
    Olsson, P.
    Lund Univ, Sweden.
    Wollmer, P.
    Lund Univ, Sweden.
    Mandl, T.
    Lund Univ, Sweden.
    Increased B-cell activating factor, interleukin-6, and interleukin-8 in induced sputum from primary Sjogrens syndrome patients2019In: Scandinavian Journal of Rheumatology, ISSN 0300-9742, E-ISSN 1502-7732, Vol. 48, no 2, p. 149-156Article in journal (Refereed)
    Abstract [en]

    Objective: Small airway disease and chronic obstructive pulmonary disease are common in primary Sjogrens syndrome (pSS). However, the underlying inflammatory mechanisms behind pSS-associated airway disease have not been studied in detail. We therefore wanted to study cytokine and leucocyte levels in induced sputum in never-smoking patients with pSS. Method: Induced sputum cytokines and leucocytes were assessed in 20 never-smoking patients with pSS and 19 age- and gender-matched population-based controls. In addition, pulmonary function, disease activity, respiratory symptoms, and inflammatory and serological features of pSS were assessed. Results: B-cell activating factor (BAFF), interleukin-6 (IL-6) and IL-8 were significantly increased in induced sputum in pSS patients compared to population-based controls, while IL-1 beta, interferon-alpha, and tumour necrosis factor-alpha levels and leucocytes were not. The proportion of lymphocytes and BAFF levels in induced sputum correlated significantly in pSS patients. However, cytokine levels in induced sputum were not associated with pulmonary function tests, disease activity, respiratory symptoms, or serological features of pSS. Conclusion: The increase in BAFF, IL-6, and IL-8 in induced sputum suggests a specific ongoing inflammatory disease process in the airways in pSS patients. Its association with pSS-associated airway disease needs to be further examined in future larger studies.

  • 24.
    Nilsson, Lennart
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Brockow, Knut
    Technical University Munich, Munich, Germany.
    Alm, Johan
    Karolinska Institutet, Södersjukhuset, Stockholm, Sweden.
    Cardona, Victoria
    Hospital Universitari Vall d'Hebron, Barcelona, Spain.
    Caubet, Jean-Christoph
    University of Geneva, Genève, Switzerland.
    Gomes, Eva
    CHP, Porto, Portugal.
    Jenmalm, Maria Christina
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Lau, Susanne
    Charité Universitätsmedizin, Berlin, Germany.
    Netterlid, Eva
    Lund University, Malmö, The Public Health Agency of Sweden, Stockholm, Sweden.The University of Edinburgh, Edinburgh, UK.
    Schwarze, Jürgen
    The University of Edinburgh, Edinburgh, UK.
    Sheikh, Aziz
    The University of Edinburgh, Edinburgh, UK..
    Storsaeter, Jann
    Norwegian Institute of Public Health, Oslo, Norway.
    Skevaki, Chrysanthi
    Philipps University Marburg, University Hospital Giessen and Marburg GmbH, Marburg, Germany.
    Terreehorst, Ingrid
    Department of ENT, AMC, Amsterdam, the Netherlands.
    Zanoni, Giovanna
    Immunology Unit, University Hospital, Verona, Italy.
    Vaccination and allergy: EAACI position paper, practical aspects2017In: Pediatric Allergy and Immunology, ISSN 0905-6157, E-ISSN 1399-3038Article, review/survey (Refereed)
    Abstract [en]

    Immunization is highly effective in preventing infectious diseases and therefore an indispensable public health measure. Allergic patients deserve access to the same publicly recommended immunizations as nonallergic patients unless risks associated with vaccination outweigh the gains. Whereas the number of reported possible allergic reactions to vaccines is high, confirmed vaccine-triggered allergic reactions are rare. Anaphylaxis following vaccination is rare, affecting less than 1/100,000, but can occur in any patient. Some patient groups, notably those with a previous allergic reaction to a vaccine or its components, are at heightened risk of allergic reaction and require special precautions. Allergic reactions, however, may occur in patients without known risk factors and cannot be predicted by currently available tools. Unwarranted fear and uncertainty can result in incomplete vaccination coverage for children and adults with or without allergy. In addition to concerns about an allergic reaction to the vaccine itself, there is fear that routine childhood immunization may promote the development of allergic sensitization and disease. Thus, although there is no evidence that routine childhood immunization increases the risk of allergy development, such risks need to be discussed. This article is protected by copyright. All rights reserved.

  • 25.
    Nyström Kronander, Ulla
    et al.
    Region Östergötland, Heart and Medicine Center, Allergy Center.
    Ahlbeck, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Atopi, allergi och överkänslighet2018In: Läkemedelsboken, Läkemedelsverket , 2018Chapter in book (Other academic)
  • 26.
    Nyström, Ulla
    et al.
    Region Östergötland, Heart and Medicine Center, Allergy Center.
    Ahlbeck, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Allergi och annan överkänslighet2018In: Internmedicin / [ed] Ulf Dahlström, Stergios Kechagias, Leif Stenke, Liber, 2018, 6, p. 31-58Chapter in book (Other academic)
  • 27.
    Persson, Lennart
    et al.
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    Lyth, Johan
    Linköping University, Department of Medical and Health Sciences, Division of Health Care Analysis. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Regional Board, Research and Development Unit.
    Wiréhn, Ann-Britt
    Linköping University, Department of Medical and Health Sciences, Division of Health Care Analysis. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Regional Board, Research and Development Unit.
    Lind, Leili
    Linköping University, Department of Biomedical Engineering, Division of Biomedical Engineering. Linköping University, Faculty of Science & Engineering.
    Elderly patients with COPD require more health care than elderly heart failure patients do in a hospital-based home care setting2019In: The International Journal of Chronic Obstructive Pulmonary Disease, ISSN 1176-9106, E-ISSN 1178-2005, Vol. 14, p. 1569-1581Article in journal (Refereed)
    Abstract [en]

    Background: Elderly patients with advanced stages of COPD or chronic heart failure (CHF) often require hospitalization due to exacerbations. We hypothesized that telemonitoring supported by hospital-based home care (HBHC) would detect exacerbations early, thus, reducing the number of hospitalization. We also speculated that patients with advanced COPD or CHF would present differences regarding exacerbation frequency and the need of HBHC. Methods: The Health Diary system, based on digital pen technology, was employed. Patients aged amp;gt;= 65 years with amp;gt;= 2 hospitalizations the previous year were included. Exacerbations were categorized and treated as either COPD or CHF exacerbation by an experienced physician. All HBHC contacts (home visits or telephone consultations) were registered. Results: Ninety-four patients with advanced diseases were enrolled (36 COPD and 58 CHF subjects) of which 53 subjects (19 COPD and 34 CHF subjects) completed the 1-year study period. Death was the major reason for not finalizing the study. Compared to the 1-year prior inclusion, the intervention significantly reduced hospitalization. Although COPD subjects were younger with less comorbidity, exacerbations and HBHC contacts were significantly greater in this group. Conclusions: COPD subjects exhibit exacerbations more frequently, mainly due to disease characteristics, thus, demanding much more HBHC.

  • 28.
    Piltén, Carina
    et al.
    Intensive Care Unit, Capio S:t Gorans Hospital, Stockholm.
    Eldh, Ann Catrine
    Intensive Care Unit, Capio S:t Gorans Hospital, Stockholm.
    Lung recruitment--a nurse and/or physician task. A national survey on requirements for education, regulations and guidelines.2009In: Intensive & Critical Care Nursing, ISSN 0964-3397, E-ISSN 1532-4036, Vol. 25, no 1, p. 4-9Article in journal (Refereed)
    Abstract [en]

    International and national guidelines on requirements for performing lung recruitment manoeuvres are lacking. This paper presents a nationwide descriptive survey of the occurrence of and conditions for lung recruitment in adult patients treated with mechanical ventilation in intensive care units (ICUs) in Sweden. All ICUs except neurological, cardiac, paediatric and neonatal ICUs were invited (N=73); of these, 60 ICUs participated in the study (82%). The main outcome measures were prevalence of lung recruitment, whether ICU nurses and/or physicians carried out lung recruitment, requirements for nurses to perform lung recruitment and the existence of local guidelines. Lung recruitment was performed at 92% of the ICUs. Only physicians performed lung recruitment at 27 ICUs (49%), and in 28 units (51%) both physicians and nurses performed this treatment. Lung recruitment was performed more often in units where both physicians and nurses performed lung recruitment than in units where only physicians performed the manoeuvres (46% vs. 12%, p=0.03). Further, local guidelines on lung recruitment manoeuvres were more common in units where both physicians and nurses performed this treatment (71% vs. 41%, p=0.02). The results suggest that recommendations of repeated and prompt lung recruitment manoeuvres are better met if nurses, along with physicians, perform lung recruitment.

  • 29.
    Portugues, Cyril
    et al.
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Crespo-Picazo, Jose Luis
    Fdn Oceanog Comunidad Valenciana, Spain.
    Garcia-Parraga, Daniel
    Fdn Oceanog Comunidad Valenciana, Spain.
    Altimiras, Jordi
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Lorenzo, Teresa
    Fdn Oceanog Comunidad Valenciana, Spain.
    Borque-Espinosa, Alicia
    Fdn Oceanog Comunidad Valenciana, Spain; Univ Valencia, Spain; Hosp Univ and Politecn La Fe, Spain.
    Fahlman, Andreas
    Fdn Oceanog Comunidad Valenciana, Spain; Hosp Univ and Politecn La Fe, Spain.
    Impact of gas emboli and hyperbaric treatment on respiratory function of loggerhead sea turtles (Caretta caretta)2018In: Conservation Physiology, E-ISSN 2051-1434, Vol. 6, article id cox074Article in journal (Refereed)
    Abstract [en]

    Fisheries interactions are the most serious threats for sea turtle populations. Despite the existence of some rescue centres providing post-traumatic care and rehabilitation, adequate treatment is hampered by the lack of understanding of the problems incurred while turtles remain entrapped in fishing gears. Recently it was shown that bycaught loggerhead sea turtles (Caretta caretta) could experience formation of gas emboli (GE) and develop decompression sickness (DCS) after trawl and gillnet interaction. This condition could be reversed by hyperbaric O-2 treatment (HBOT). The goal of this study was to assess how GE alters respiratory function in bycaught turtles before recompression therapy and measure the improvement after this treatment. Specifically, we assessed the effect of DCS on breath duration, expiratory and inspiratory flow and tidal volume (VT), and the effectiveness of HBOT to improve these parameters. HBOT significantly increased respiratory flows by 32-45% while VT increased by 33-35% immediately after HBOT. Repeated lung function testing indicated a temporal increase in both respiratory flow and VT for all bycaught turtles, but the changes were smaller than those seen immediately following HBOT. The current study suggests that respiratory function is significantly compromised in bycaught turtles with GE and that HBOT effectively restores lung function. Lung function testing may provide a novel means to help diagnose the presence of GE, be used to assess treatment efficacy, and contribute to sea turtle conservation efforts.

  • 30.
    Senti, Gabriela
    et al.
    Clinical Trials Center, University Hospital, Zurich, Switzerland.
    Freiburghaus, Andreas U.
    Clinical Trials Center, University Hospital, Zurich, Switzerland.
    Larenas-Linnemann, Désirée
    Hospital Médica Sur, Mexico City, Mexico.
    Hoffmann, Hans Jürgen
    Department of Clinical Medicine, Aarhus University, Denmark; Department of Respiratory Diseases and Allergy, Aarhus University Hospital, Denmark.
    Patterson, Amber M.
    ENT & Allergy Specialists of Northwest Ohio, USA.
    Klimek, Ludger
    Center for Rhinology and Allergology, Germany.
    Di Bona, Danilo
    Department of Emergency and Organ Transplantation, Chair and School of Allergology and Clinical Immunology, University of Bari – Aldo Moro, Italy.
    Pfaar, Oliver
    Center for Rhinology and Allergology, Germany; Department of Otorhinolaryngology, Head and Neck Surgery, Universitätsmedizin Mannheim, Medical Faculty Mannheim, Heidelberg University, Germany.
    Ahlbeck, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Akdis, Mübeccel
    Swiss Institute of Allergy and Asthma Research SIAF, Switzerland.
    Weinfeld, Dan
    Asthma and Allergy Clinic (Adults), Department of Internal Medicine, South Alvsborgs (Central) Hospital, Sweden.
    Contreras-Verduzco, Francisco A.
    Allergy Department, National Institute of Pediatrics, Mexico.
    Pedroza-Melendez, Alvaro
    Allergy Department, National Institute of Pediatrics, Mexico.
    Skaarup, Søren H.
    Department of Clinical Medicine – Department of Respiratory Diseases and Allergy, Aarhus University, Denmark.
    Lee, Sang Min
    Division of Allergy and Pulmonology, Department of Internal Medicine, Gil Medical Center, Gachon University College of Medicine, Republic of Korea.
    Cardell, Lars-Olaf
    Division of ENT Diseases, Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Sweden.
    Schmid, Johannes M.
    Department of Respiratory Diseases and Allergy, Aarhus University Hospital, Denmark.
    Westin, Ulla
    Division of Ear, Nose and Throat Diseases, Head and Neck Surgery, Department of Clinical Sciences, Lund University, Skane University Hospital, Sweden; Region Skane, Skane University Hospital, Sweden.
    Dollner, Ralph
    Department Otorhinolaryngology – Head and Neck Surgery, Clinic for Head-Neck and Reconstructive Surgery, Oslo University Hospital (OUS) HF – Rikshospitalet, Oslo, Norway.
    Kündig, Thomas M.
    Department of Dermatology, University Hospital Zurich, Switzerland.
    Intralymphatic Immunotherapy: Update and Unmet Needs.2019In: International Archives of Allergy and Immunology, ISSN 1018-2438, E-ISSN 1423-0097, Vol. 178, no 2, p. 141-149Article, review/survey (Refereed)
    Abstract [en]

    Allergen-specific immunotherapy (AIT) is the only allergy treatment that confers long-term symptom amelioration for patients suffering from allergy. The most frequently used allergen application route is subcutaneous injection (SCIT), commonly taken as the gold standard, followed by sublingual (SLIT) or oral (OIT) application of allergen preparations. This is an up-to-date review of the clinical evidence for a novel route of allergen application, i.e., directly into lymph nodes - intralymphatic immunotherapy (ILIT). The major advantages of ILIT over the current AIT approaches are its short duration and the low allergen doses administered. The whole treatment consists of merely 3 ultrasound-guided injections into inguinal lymph nodes 1 month apart. While the number of patients included in randomised controlled trials is still limited, the clinical results for ILIT are encouraging, but more clinical trials are needed, as well as more preclinical work for optimising formulations.

  • 31.
    Sköld, Carl Magnus
    et al.
    Department of Medicine Solna, Karolinska Institutet, Lung-Allergy Clinic, Karolinska University Hospital Solna, Stockholm, Sweden.
    Janson, Christer
    Department of Medical Sciences: Respiratory, Allergy and Sleep Research, Uppsala University, Uppsala, Sweden.
    Klackenberg Elf, Åsa
    InterMune Nordics AB, Stockholm, Sweden; Roche AB, Stockholm, Sweden.
    Fiaschi, Marie
    Roche AB, Stockholm, Sweden.
    Wiklund, Kerstin
    PCG Clinical Services, Uppsala, Sweden.
    Persson, Hans Lennart
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    A retrospective chart review of pirfenidone-treated patients in Sweden: the REPRIS study2016In: European Clinical Respiratory Journal, E-ISSN 2001-8525, Vol. 3, no 1, article id 32035Article in journal (Refereed)
    Abstract [en]

    Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that usually results in respiratory failure and death. Pirfenidone was approved as the first licensed therapy for IPF in Europe based on phase III trials where patients with a forced vital capacity (FVC) greater than50% of predicted were included. The aim of this study was to characterise patients treated with pirfenidone in Swedish clinical practice and to describe the adherence to the reimbursement restriction since reimbursement was only applied for patients with FVC below 80% of predicted.less thanbr /greater thanMethods: This was a retrospective, observational chart review of IPF patients treated with pirfenidone from three Swedish university clinics. Patients initiated on treatment during the period 28 June 2012 to 20 November 2014 were included. Data on patient characteristics, basis of diagnosis, treatment duration, quality of life, and adverse drug reactions (ADRs) were collected from medical charts.less thanbr /greater thanResults: Forty-four patients were screened and 33 were included in the study. The mean treatment duration from start of pirfenidone until discontinuation or end of study was 38 weeks. At the initiation of pirfenidone treatment, FVC was 62.7% (12.1) [mean (SD)], diffusion capacity (DLco) was 45.1% (13.8) of predicted, and the ratio of forced expiratory volume on 1 sec (FEV1) to FVC was 0.78 (0.1). The percentage of patients with an FVC between 50 and 80% was 87%. Ten of the patients had ADRs including gastrointestinal and skin-related events, cough and signs of impaired hepatic function, but this led to treatment discontinuation in only two patients.less thanbr /greater thanConclusion: Data from this chart review showed that adherence to the Swedish reimbursement restriction was followed in the majority of patients during the study period. At the start of pirfenidone treatment, lung function, measured as FVC, was lower in the present cohort of Swedish IPF patients compared with other registry and real-life data. About a third of the patients had ADRs, but discontinuation of the treatment because of ADRs was relatively uncommon.

  • 32.
    Stridh, Björn
    et al.
    Kista vårdcentral, Stockholm, Sweden.
    Romberg, K.
    Näsets Läkargrupp, Höllviken, Sweden; Kunskapscentrum för allergi, astma och KOL, Skånes universitetssjukhus, Lund, Sweden.
    Ställberg, Björn
    Institutionen för folkhälso- och vårdvetenskap, allmänmedicin och preventivmedicin, Uppsala universitet, Uppsala, Sweden.
    Ahlbeck, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Kiotseridis, Hampus
    Barnläkargruppen Sparta, Lund, Sweden; Institutionen för lungmedicin och allergologi, Lunds universitet, Lund, Sweden.
    Janson, Christer
    Institutionen för medicinska vetenskaper, Uppsala universitet, Uppsala, Sweden.
    Många överbehandlas med astmamedicin [When and how to step down asthma treatment]2018In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 115Article in journal (Refereed)
  • 33.
    Ställberg, B.
    et al.
    Trosa Health Care Centre, Trosa, Sweden, Dept. of Public Health/Caring Sci., University of Uppsala, Uppsala, Sweden.
    Nyström Kronander, Ulla
    Linköping University, Department of Clinical and Experimental Medicine, Allergy Centre. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Allergy Center.
    Olsson, P.
    Sjöbo Health Care Centre, Sjöbo, Sweden.
    Gottberg, L.
    Dept. Respiratory Medicine/Allergy, University Hospital of Huddinge, Huddinge, Sweden.
    Rönmark, E.
    The OLIN Studies, Sunderby Central Hosp. of Norrbotten, Luleå, Sweden, Dept. Respiratory Medicine/Allergy, University of Umeå, Umeå, Sweden, Lung and Allergy Research, National Institute of Environ. Med., Karolinska Institute, Stockholm, Sweden.
    Lundbäck, B.
    The OLIN Studies, Sunderby Central Hosp. of Norrbotten, Luleå, Sweden, Lung and Allergy Research, National Institute of Environ. Med., Karolinska Institute, Stockholm, Sweden.
    Living with asthma in Sweden - The ALMA study2003In: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 97, no 7, p. 835-843Article in journal (Refereed)
    Abstract [en]

    Background: Recently performed studies have found a number of limitations in the daily lives of asthmatics, and a large disparity between the perception of the sufferers and what health care professionals believe matters to asthmatics. Aim: What matters to Swedish asthma patients, what medicines do they use, and are they compliant with given prescriptions? A further aim was to compare perceptions about asthma and asthma management in asthmatics and among Swedish general practitioners (GP). Design: A structured telephone interview of a representative sample of Swedish asthmatics, and a mailed questionnaire survey among GPs from different parts of Sweden. Methods: Screening by telephone of a random sample of 10,350 subjects aged 18-45. Of those, 240 were subsequently selected for a detailed structured telephone interview about their asthma. A mailed structured questionnaire containing similar questions to those asked of the asthmatics was sent to 600 GPs, and 139 returned completed answers. Results: 16% of the asthmatics reported (asthma) symptoms occurring every day during the previous month. Nocturnal symptoms at least twice per week were reported by 19%. Both these were reported by considerably higher proportions of the asthmatics than the GPs had expected. A large majority classified their disease as mild or very mild, although great majority reported frequent symptoms. Activities or situations which caused symptoms of asthma often or "now and then" were physical exertion, 67%, bad weather, 59%, contact with animals/pets, 58%, and visits to cafés or restaurants, 36%, and several asthmatics avoided these activities due to their asthma. Conclusion: A great majority of asthmatics report a large number of symptoms and limitations in their daily living in proportions which were roughly expected by the GPs. © 2003 Elsevier Science Ltd. All rights reserved.

  • 34.
    Toren, K.
    et al.
    University of Gothenburg, Sweden.
    Bake, B.
    University of Gothenburg, Sweden.
    Olin, A-C
    University of Gothenburg, Sweden.
    Engstrom, G.
    Lund University, Sweden.
    Blomberg, A.
    Umeå University, Sweden.
    Vikgren, J.
    University of Gothenburg, Sweden.
    Hedner, J.
    University of Gothenburg, Sweden.
    Brandberg, J.
    University of Gothenburg, Sweden.
    Persson, Lennart
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Respiratory Medicine.
    Sköld, C. M.
    Karolinska Institute, Sweden.
    Rosengren, A.
    University of Gothenburg, Sweden.
    Bergstrom, G.
    University of Gothenburg, Sweden.
    Janson, C.
    Uppsala University, Sweden.
    Measures of bronchodilator response of FEV1, FVC and SVC in a Swedish general population sample aged 50-64 years, the SCAPIS Pilot Study2017In: The International Journal of Chronic Obstructive Pulmonary Disease, ISSN 1176-9106, E-ISSN 1178-2005, Vol. 12, p. 973-980Article in journal (Refereed)
    Abstract [en]

    Background: Data are lacking from general population studies on how to define changes in lung function after bronchodilation. This study aimed to analyze different measures of bronchodilator response of forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC) and slow vital capacity (SVC). Materials and methods: Data were derived from the Swedish Cardiopulmonary Bioimage Study (SCAPIS) Pilot study. This analysis comprised 1,050 participants aged 50-64 years from the general population. Participants were investigated using a questionnaire, and FEV1, FVC and SVC were recorded before and 15 minutes after inhalation of 400 mu g of salbutamol. A bronchodilator response was defined as the relative change from baseline value expressed as the difference in units of percent predicted normal. Predictors of bronchodilator responses were assessed using multiple linear regression models. Airway obstruction was defined as FEV1/FVC ratio below lower limit of normal (LLN) before bronchodilation, and COPD was defined as an FEV1/FVC ratio below LLN after bronchodilation. Physician-diagnosed asthma was defined as an affirmative answer to " Have you ever had asthma diagnosed by a physician?". Asymptomatic never-smokers were defined as those not reporting physician-diagnosed asthma, physician-diagnosed COPD or emphysema, current wheeze or chronic bronchitis and being a lifelong never-smoker. Results: Among all subjects, the greatest bronchodilator responses (FEV1, FVC and SVC) were found in subjects with asthma or COPD. The upper 95th percentile of bronchodilator responses in asymptomatic never-smokers was 8.7% for FEV1, 4.2% for FVC and 5.0% for SVC. The bronchodilator responses were similar between men and women. In a multiple linear regression model comprising all asymptomatic never-smokers, the bronchodilator response of FEV1 was significantly associated with airway obstruction and height. Conclusion: When the bronchodilator response in asymptomatic never-smokers is reported as the difference in units of predicted normal, significant reversibility of FEV1, FVC and SVC to bronchodilators is 9%, 4% and 5%, respectively.

  • 35.
    Torres, Antoni
    et al.
    University of Barcelona, Spain; CIBERES, Spain.
    Niederman, Michael S.
    Weill Cornell Med, NY USA.
    Chastre, Jean
    Grp Hospital Pitie Salpetriere, France.
    Ewig, Santiago
    Evangel Hospital Herne, Germany; Augusta Hospital Bochum, Germany.
    Fernandez-Vandellos, Patricia
    CIBERES, Spain.
    Hanberger, Håkan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Infectious Diseases.
    Kollef, Marin
    Washington University, MO USA.
    Li Bassi, Gianluigi
    University of Barcelona, Spain; CIBERES, Spain.
    Luna, Carlos M.
    University of Buenos Aires, Argentina.
    Martin-Loeches, Ignacio
    Trinity Coll Dublin, Ireland; CIBERES, Spain.
    Artur Paiva, J.
    University of Porto, Portugal; University of Porto, Portugal.
    Read, Robert C.
    University of Southampton, England; University of Southampton, England; University of Southampton, England.
    Rigau, David
    Iberoamer Cochrane Centre, Spain.
    Francois Timsit, Jean
    Paris Diderot University, France; Hop Xavier Bichat, France.
    Welte, Tobias
    Hannover Medical Sch, Germany; German Centre Lung Research DZL, Germany.
    Wunderink, Richard
    Northwestern University, IL 60611 USA.
    International ERS/ESICM/ESCMID/ALAT guidelines for the management of hospital-acquired pneumonia and ventilator-associated pneumonia2017In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 50, no 3, article id 1700582Article in journal (Refereed)
    Abstract [en]

    The most recent European guidelines and task force reports on hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) were published almost 10 years ago. Since then, further randomised clinical trials of HAP and VAP have been conducted and new information has become available. Studies of epidemiology, diagnosis, empiric treatment, response to treatment, new antibiotics or new forms of antibiotic administration and disease prevention have changed old paradigms. In addition, important differences between approaches in Europe and the USA have become apparent. The European Respiratory Society launched a project to develop new international guidelines for HAP and VAP. Other European societies, including the European Society of Intensive Care Medicine and the European Society of Clinical Microbiology and Infectious Diseases, were invited to participate and appointed their representatives. The Latin American Thoracic Association was also invited. A total of 15 experts and two methodologists made up the panel. Three experts from the USA were also invited (Michael S. Niederman, Marin Kollef and Richard Wunderink). Applying the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) methodology, the panel selected seven PICO (population-intervention-comparison-outcome) questions that generated a series of recommendations for HAP/VAP diagnosis, treatment and prevention.

  • 36.
    Winkler, Carla
    et al.
    AstraZeneca, Sweden.
    Hochdoerfer, Thomas
    AstraZeneca, Sweden.
    Israelsson, Elisabeth
    AstraZeneca, Sweden.
    Hasselberg, Annemarie
    AstraZeneca, Sweden.
    Cavallin, Anders
    AstraZeneca, Sweden.
    Thoern, Kristofer
    AstraZeneca, Sweden.
    Muthas, Daniel
    AstraZeneca, Sweden.
    Shojaee, Shervin
    AstraZeneca, Sweden.
    Lueer, Katrin
    Fraunhofer Inst Toxicol and Expt Med, Germany.
    Mueller, Meike
    Fraunhofer Inst Toxicol and Expt Med, Germany.
    Mjösberg, Jenny
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Karolinska Inst, Sweden.
    Vaarala, Outi
    AstraZeneca, Sweden.
    Hohlfeld, Jens
    Fraunhofer Inst Toxicol and Expt Med, Germany; German Ctr Lung Res BREATH, Germany; Hannover Med Sch, Germany.
    Pardali, Katerina
    AstraZeneca, Sweden.
    Activation of group 2 innate lymphoid cells after allergen challenge in asthmatic patients2019In: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 144, no 1, p. 61-+Article in journal (Refereed)
    Abstract [en]

    Background: Group 2 innate lymphoid cells (ILC2s) are effective producers of IL-5 and IL-13 during allergic inflammation and bridge the innate and adaptive immune responses. ILC2 numbers are increased in asthmatic patients compared with healthy control subjects. Thus far, human data describing their phenotype during acute allergic inflammation in the lung are incomplete. Objectives: This study aims to characterize and compare blood and lung-derived ILC2s before and after segmental allergen challenge in patients with mild-to-moderate asthma with high blood eosinophil counts (amp;gt;= 300 cells/mu L). Methods: ILC2s were isolated from blood and bronchoalveolar lavage (BAL) fluid before and after segmental allergen challenge. Cells were sorted by means of flow cytometry, cultured and analyzed for cytokine release or migration, and sequenced for RNA expression. Results: ILC2s were nearly absent in the alveolar space under baseline conditions, but numbers increased significantly after allergen challenge (P amp;lt; .05), whereas at the same time, ILC2 numbers in blood were reduced (P amp;lt; .05). Prostaglandin D2 and CXCL12 levels in BAL fluid correlated with decreased ILC2 numbers in blood (P = .004, respective P = .024). After allergen challenge, several genes promoting type 2 inflammation were expressed at greater levels in BAL fluid compared with blood ILC2s, whereas blood ILC2s remain unactivated. Conclusion: ILC2s accumulate at the site of allergic inflammation and are recruited from the blood. Their transcriptional and functional activation pattern promotes type 2 inflammation.

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