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  • 1.
    Benson, Mikael
    et al.
    Queen Silvia Children's Hospital, Gothenburg, Sweden.
    Fransson, M.
    Laboratory for Clinical and Experimental Allergy Research, Department of Oto-Rhino-Laryngology, Malmö University Hospital, Malmö, Sweden.
    Martinsson, T.
    Department of Clinical Genetics, Gothenburg, Sweden.
    Naluai, Å.T.
    Department of Clinical Genetics, Gothenburg, Sweden.
    Uddman, R.
    Laboratory for Clinical and Experimental Allergy Research, Department of Oto-Rhino-Laryngology, Malmö University Hospital, Malmö, Sweden.
    Cardell, L. O.
    Laboratory for Clinical and Experimental Allergy Research, Department of Oto-Rhino-Laryngology, Malmö University Hospital, Malmö, Sweden.
    Inverse relation between nasal fluid Clara Cell Protein 16 levels and symptoms and signs of rhinitis in allergen-challenged patients with intermittent allergic rhinitis2007Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 62, nr 2, s. 178-183Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Decreased levels of the anti-inflammatory Clara Cell Protein 16 (CC16) are found in intermittent allergic rhinitis (IAR) and asthma. In asthma this decrease has been associated with hyperreactivity and the A38G single nucleotide polymorphism (SNP). The aim of this study was to examine if IAR is associated with signs and symptoms of rhinitis and the A38G SNP.

    METHODS: Nasal fluid CC16 was analyzed in 20 patients with IAR before allergen challenge and 1 and 6 h after challenge, and from 28 healthy controls. The A38G SNP was analyzed in 80 patients with IAR and 106 controls. Nasal biopsies were obtained from three subjects in each group for immunohistochemical analysis of CC16.

    RESULTS: In the allergen-challenged patients symptoms and rhinoscopic signs of rhinitis increased after 1 h and normalized after 6 h. In contrast, nasal fluid CC16 decreased 1 h after allergen challenge and returned to baseline after 6 h. Nasal fluid CC16 levels did not differ from controls before and 6 h after challenge. Immunohistochemical investigation showed intense CC16 staining in the nasal epithelium of both patients before season and healthy controls, but weak staining in symptomatic patients during season. No significant association between the A38G SNP and IAR was found.

    CONCLUSION: There was an inverse relation between nasal fluid CC16 levels and symptoms and signs of rhinitis in allergen-challenged patients with IAR. However, there was no association between IAR and the A38G SNP.

  • 2.
    Benson, Mikael
    et al.
    Unit for Clinical Systems Biology, Department of Pediatrics, Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Mobini, R.
    Unit for Clinical Systems Biology, Department of Pediatrics, Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Barrenäs, F.
    Unit for Clinical Systems Biology, Department of Pediatrics, Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Halldén, C.
    Department of Clinical Chemistry, Malmö University Hospital, Malmö, Sweden.
    Naluai, Å.T.
    Department of Clinical Genetics, Sahlgrenska Academy, Gothenburg, Sweden.
    Säll, T.
    Department of Cell and Organism Biology, Lund University, Lund, Sweden.
    Cardell, L.O.
    Division of ENT diseases Huddinge, CLINTEC, Karolinska Institutet, Stockholm, Sweden.
    A haplotype in the inducible T-cell tyrosine kinase is a risk factor for seasonal allergic rhinitis2009Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 64, nr 9, s. 1286-1291Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Identification of disease-associated single nucleotide polymorphisms (SNPs) in seasonal allergic rhinitis (SAR) may be facilitated by focusing on genes in a disease-associated pathway.

    OBJECTIVE: To search for SNPs in genes that belong to the T-cell receptor (TCR) pathway and that change in expression in allergen-challenged CD4+ cells from patients with SAR.

    METHODS: CD4+ cells from patients with SAR were analysed with gene expression microarrays. Allele, genotype and haplotype frequencies were compared in 251 patients and 386 healthy controls.

    RESULTS: Gene expression microarray analysis of allergen-challenged CD4+ cells from patients with SAR showed that 25 of 38 TCR pathway genes were differentially expressed. A total of 62 SNPs were analysed in eight of the 25 genes; ICOS, IL4, IL5, IL13, CSF2, CTLA4, the inducible T-cell tyrosine kinase (ITK) and CD3D. Significant chi-squared values were identified for several markers in the ITK kinase gene region. A total of five SNPs were nominally significant at the 5% level. Haplotype analysis of the five significant SNPs showed increased frequency of a haplotype that covered most of the coding part of ITK. The functional relevance of ITK was supported by analysis of an independent material, which showed increased expression of ITK in allergen-challenged CD4+ cells from patients, but not from controls.

    CONCLUSION: Analysis of SNPs in TCR pathway genes revealed that a haplotype that covers a major part of the coding sequence of ITK is a risk factor for SAR.

  • 3.
    Benson, Mikael
    et al.
    Malmö University Hospital, Sweden .
    Reinholdt, J
    Royal Dental College, Aarhus, Denmark.
    Cardell, L O
    Malmö University Hospital, Sweden.
    Allergen-reactive antibodies are found in nasal fluids from patients with birch pollen-induced intermittent allergic rhinitis, but not in healthy controls2003Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 58, nr 5, s. 386-392Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Increased levels of allergen-reactive immunoglobulins (Igs) have been reported in nasal fluids from patients with intermittent allergic rhinitis (IAR) sensitive to ragweed and grass. The aims of this study were to make a detailed characterization of nasal fluid Igs in birch pollen-induced IAR.

    METHODS: Nasal fluids were obtained from 23 patients with birch pollen-induced IAR during and after the birch pollen season, and from 20 healthy controls. Nasal fluid total and Bet v 1-reactive (IgA), IgE and IgG as well as albumin were analyzed by immunoassays. The integrity of IgA and IgG, and the molecular form of IgA were assessed by Western blotting and column fractionation, respectively.

    RESULTS: Nasal fluid total IgE and IgG, but not IgA, were higher in patients compared with controls. Western blotting indicated no significant degradation of IgA (including S-IgA) and IgG. Most of the IgA, including Bet v 1-reactive antibodies, was of the secretory form and of the IgA1 subclass. Bet v 1-reactive IgA and IgG were present in all patients, but was mostly nondetectable in controls. No significant differences in the levels of Bet v 1-reactive IgA and IgG were found in patients during the birch pollen season compared with off season. Both Bet v 1 and Bet v 2-reactive IgE were nondetectable in most samples.

    CONCLUSIONS: Nasal fluid Bet v 1-reactive IgA and IgG were found in all patients with birch pollen-induced IAR, but not in controls. However, no significant differences were found between patients during and after the birch pollen season.

  • 4.
    Björkstén, B
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    The environmental influence on childhood asthma. 1999Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 54, s. 17-23Artikel i tidskrift (Refereegranskat)
  • 5.
    Bogefors, J.
    et al.
    Department of Otorhinolaryngology, Malmö University Hospital, Lund University, Malmö, Sweden.
    Rydberg, C.
    Division of ENT diseases, CLINTEC, Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Uddman, R.
    Department of Otorhinolaryngology, Malmö University Hospital, Lund University, Malmö, Sweden.
    Fransson, M.
    Department of Otorhinolaryngology, Malmö University Hospital, Lund University, Malmö, Sweden.
    Månsson, A.
    Division of ENT diseases, CLINTEC, Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Benson, Mikael
    Unit for Clinical Systems Biology, Department of Pediatrics, Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Adner, M.
    National Institute of Environmental medicine, Karolinska Institutet, Stockholm, Sweden.
    Cardell, Lars Olaf
    Division of ENT diseases, CLINTEC, Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Nod1, Nod2 and Nalp3 receptors, new potential targets in treatment of allergic rhinitis?2010Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 65, nr 10, s. 1222-1226Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Recently, a new set of pattern-recognition receptors, the nucleotide-binding oligomerization domain (Nod)-like receptors (NLRs), have emerged. Their activation, either by allergens or microbes, triggers an inflammatory response. The knowledge about NLRs in human airways is limited.

    AIM OF THE STUDY: To investigate presence of NLRs in the human nose of healthy individuals and patients with intermittent allergic rhinitis outside and during pollen season.

    METHODS: The expression of Nod1, Nod2, and Nalp3 in nasal biopsies was determined with real-time RT-PCR and immunohistochemistry. Cultured primary human nasal epithelial cells (HNECs) were analyzed using real-time RT-PCR and flow cytometry to further verify the presence of NLRs in the epithelium.

    RESULTS: Immunohistochemical analysis revealed presence of Nod1, Nod2, and Nalp3 in the nasal epithelium. This was corroborated in cultured HNECs. Patients suffering from symptomatic allergic rhinitis exhibited lower Nod1 and Nalp3 mRNA levels than both controls and patients during pollen season. Nod2 expression was found in all specimens tested, but no differences were seen between the three groups.

    CONCLUSION: Nod1, Nod2, and Nalp3 receptors were found to be present in the human nose. The expression of Nod1 and Nalp3 were down-regulated during pollen season among patients with allergic rhinitis. This opens up for new insights and novel therapeutic strategies in inflammatory airway disease.

  • 6.
    Borres, Magnus P.
    et al.
    Department of Pediatrics, Sahlgrenska Academy of Göteborg University, Göteborg, Sweden/Phadia AB, Uppsala, Sweden.
    Irander, Kristina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Björkstén, Bengt
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Nasal metachromatic cells in infancy in relation to the appearance of atopic disease during the first 6 years of life1997Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 52, nr 7, s. 770-774Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The relationship between the appearance of nasal metachromatic cells (basophils and mast cells) during the first 18 months of life and the development of respiratory and other allergic diseases up to 6 years of age was studied prospectively in 67 children. Follow-up was done at 3, 6, 9, and 18 months and 6 years. Of the 31 children who had detectable metachromatic cells in the nasal mucosa during infancy, 18 had atopic manifestations at 6 years (58%), two were probably atopic (6%), and 11 (36%) were nonatopic. The corresponding numbers for the 33 children without detectable metachromatic cells during infancy were 10 atopic (30%), two probably atopic (6%), and 21 nonatopic (64%) at 6 years (P<0.05). Children having detectable nasal metachromatic cells at every examination were more often allergic than children with no detectable cells at any time during the 6-year follow-up period (P<0.05). In contrast, nasal metachromatic cells were equally commonly demonstrated at 6 years in children with and without current atopic manifestations. We conclude that metachromatic cells appear at an earlier age in the nasal mucosa of atopic than nonatopic infants. The observation further supports the existence of a primary immunologic abnormality in atopic patients as related to allergic inflammatory responses. The diagnostic efficacy of this marker was too low, however, to be clinically useful as a predictor of allergy.

  • 7.
    Bousquet, J.
    et al.
    University Hospital, France; European Innovat Partnership Act and Health Ageing Re, France; INSERM, France; University of Versailles St Quentin En Yvelines UVSQ, France.
    Schunemann, H. J.
    McMaster University, Canada.
    Fonseca, J.
    University of Porto, Portugal; University of Porto, Portugal; University of Porto, Portugal; University of Porto, Portugal; University of Porto, Portugal.
    Samolinski, B.
    Medical University of Warsaw, Poland.
    Bachert, C.
    Ghent University Hospital, Belgium.
    Canonica, G. W.
    University of Genoa, Italy.
    Casale, T.
    University of S Florida, FL USA.
    Cruz, A. A.
    University of Federal Bahia, Brazil; GARD Execut Comm, Brazil.
    Demoly, P.
    Montpellier University Hospital, France; INSERM, France; UPMC, France.
    Hellings, P.
    Katholieke University of Leuven, Belgium.
    Valiulis, A.
    Vilnius University, Lithuania.
    Wickman, M.
    Sachs Childrens Hospital, Sweden; Karolinska Institute, Sweden.
    Zuberbier, T.
    Charite, Germany.
    Bosnic-Anticevitch, S.
    University of Sydney, Australia; Sydney Local Health Dist, Australia.
    Bedbrook, A.
    European Innovat Partnership Act and Health Ageing Re, France.
    Bergmann, K. C.
    Charite, Germany.
    Caimmi, D.
    Montpellier University Hospital, France.
    Dahl, R.
    Odense University Hospital, Denmark; Odense University Hospital, Denmark.
    Fokkens, W. J.
    University of Amsterdam, Netherlands.
    Grisle, I.
    Latvian Assoc Allergists, Latvia.
    Lodrup Carlsen, K.
    Oslo University Hospital, Norway; .
    Mullol, J.
    IDIBAPS, Spain.
    Muraro, A.
    Padua Gen University Hospital, Italy.
    Palkonen, S.
    EFA European Federat Allergy and Airways Disease Patien, Belgium.
    Papadopoulos, N.
    University of Manchester, England; University of Athens, Greece.
    Passalacqua, G.
    University of Genoa, Italy.
    Ryan, D.
    Woodbrook Medical Centre, England; University of Edinburgh, Scotland.
    Valovirta, E.
    University of Turku, Finland.
    Yorgancioglu, A.
    Celal Bayar University, Turkey.
    Aberer, W.
    Medical University of Graz, Austria.
    Agache, I.
    Transylvania University of Brasov, Romania.
    Adachi, M.
    Int University of Health and Welfare, Japan.
    Akdis, C. A.
    University of Zurich, Switzerland.
    Akdis, M.
    University of Zurich, Switzerland.
    Annesi-Maesano, I.
    INSERM, France; UPMC, France.
    Ansotegui, I. J.
    Hospital Quiron Bizkaia, Spain.
    Anto, J. M.
    Centre Research Environm Epidemiol, Spain; Hospital del Mar, Spain; CIBER Epidemiol and Salud Publ, Spain; University of Pompeu Fabra, Spain.
    Arnavielhe, S.
    Digi Heatlh, France.
    Arshad, H.
    David Hide Asthma and Allergy Research Centre, England.
    Baiardini, I.
    University of Genoa, Italy.
    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.
    Bel, E. H.
    University of Amsterdam, Netherlands.
    Ben Kheder, A.
    Hop Abderrahman Mami, Tunisia.
    Bennoor, K. S.
    National Institute Disease Chest and Hospital, Bangladesh.
    Benson, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Allergicentrum US.
    Bewick, M.
    Bieber, T.
    University of Bonn, Germany.
    Bindslev-Jensen, C.
    Odense University Hospital, Denmark;.
    Bjermer, L.
    University of Lund Hospital, Sweden.
    Blain, H.
    University of Montpellier, France; .
    Boner, A. L.
    University of Verona Hospital, Italy.
    Boulet, L. P.
    University of Laval, Canada.
    Bonini, M.
    University of Roma La Sapienza, Italy.
    Bonini, S.
    University of Naples 2, Italy; Italian National Research Council, Italy.
    Bosse, I.
    Bourret, R.
    Montpellier University Hospital, France.
    Bousquet, P. J.
    INSERM, France; UPMC, 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.
    University of London Imperial Coll Science Technology and Med, England; University of London Imperial Coll Science Technology and Med, England; University of London Imperial Coll Science Technology and Med, England.
    Bush, A.
    University of London Imperial Coll Science Technology and Med, England; Royal Brompton Hospital, England.
    Caballero-Fonseca, F.
    Centre Medical Docente La Trinidad, Venezuela.
    Calderon, M. A.
    University of London Imperial Coll Science Technology and Med, England.
    Camargos, P. A. M.
    University of Federal Minas Gerais, Brazil.
    Camuzat, T.
    Regional Languedoc Roussillon, France.
    Carlsen, K. H.
    Oslo University Hospital, Norway; .
    Carr, W.
    Allergy and Asthma Associates Southern Calif, CA USA.
    Cepeda Sarabia, A. M.
    University of Simon Bolivar, Colombia; SLaai, Colombia.
    Chavannes, N. H.
    Leiden University, Netherlands.
    Chiron, R.
    Montpellier University Hospital, France.
    Chkhartishvili, E.
    Grigol Robakidze University, Rep of Georgia.
    Chuchalin, A. G.
    Pulmonolory Research Institute FMBA, Russia; GARD Execut Comm, Russia.
    Ciprandi, G.
    Azienda Osped University of San Martino, Italy.
    Cirule, I.
    University of Children Hospital Latvia, Latvia.
    Correia de Sousa, J.
    University of Minho, Portugal.
    Cox, L.
    Nova SE University, FL USA.
    Crooks, G.
    NHS Scotland, Scotland.
    Costa, D. J.
    European Innovat Partnership Act and Health Ageing Re, France; Montpellier University Hospital, France.
    Custovic, A.
    University of Manchester, England.
    Dahlen, S. E.
    Karolinska Institute, Sweden.
    Darsow, U.
    Technical University of Munich, Germany.
    De Carlo, G.
    EFA European Federat Allergy and Airways Disease Patien, Belgium.
    De Blay, F.
    University Hospital Strasbourg, France.
    Deleanu, D.
    European Regional and Local Health Assoc, Belgium; Iuliu Hatieganu University of Medical and Pharm, Romania.
    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.
    Dokic, D.
    University of Skopje, Macedonia.
    Douagui, H.
    Centre Hospital University of Beni Messous, Algeria.
    Dray, G.
    Ecole Mines, France.
    Dubakiene, R.
    Vilnius State University, Lithuania.
    Durham, S. R.
    University of London Imperial Coll Science Technology and Med, England.
    Dykewicz, M. S.
    St Louis University, MI USA.
    El-Gamal, Y.
    Ain Shams University, Egypt.
    Emuzyte, R.
    Vilnius State University, Lithuania.
    Fink Wagner, A.
    Global Allergy and Asthma Platform GAAPP, Austria.
    Fletcher, M.
    Educ Heatlh, England.
    Fiocchi, A.
    Bambino Gesu Childrens Research Hospital Holy See, Italy.
    Forastiere, F.
    Regional Health Serv Lazio Reg, Italy.
    Gamkrelidze, A.
    National Centre Disease Control and Public Health Georgia, Rep of Georgia.
    Gemicioglu, B.
    Turkish Thorac Soc, Turkey.
    Gereda, J. E.
    Clin Ricardo Palma, Peru.
    Gonzalez Diaz, S.
    Sociedad Latinoamer Allergia Asma and Immunol, Mexico.
    Gotua, M.
    Georgian Assoc Allergol and Clin Immunol, Rep of Georgia.
    Grouse, L.
    University of Washington, WA USA.
    Guzman, M. A.
    University of Chile, Chile.
    Haahtela, T.
    Helsinki University Hospital, Finland.
    Hellquist-Dahl, B.
    Odense University Hospital, Denmark.
    Heinrich, J.
    Helmholtz Zentrum Munchen, Germany.
    Horak, F.
    Vienna Challenge Chamber, Austria.
    Hourihane, J. O. B.
    National University of Ireland University of Coll Cork, Ireland.
    Howarth, P.
    University of Southampton, England.
    Humbert, M.
    University of Paris 11, France; Hop Bicetre, France.
    Ivancevich, J. C.
    Clin Santa Isabel, Argentina.
    Jares, E. J.
    Libra Fdn, Argentina.
    Johnston, S. L.
    University of London Imperial Coll Science Technology and Med, England; MRC, England; Asthma UK Centre Allerg Mech Asthma, England.
    Joos, G.
    Ghent University Hospital, Belgium.
    Jonquet, O.
    Montpellier University Hospital, France.
    Jung, K. S.
    Hallym University, South Korea.
    Just, J.
    Hop Enfants Armand Trousseau, France; University of Paris 06, France.
    Kaidashev, I.
    Ukrainian Medical Stomatol Acad, Ukraine.
    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.
    Khaltaev, N.
    GARD, Switzerland.
    Klimek, L.
    Centre Rhinol and Allergol, Germany.
    Koffi NGoran, B.
    Soc Pneumol Langue Francaise, France; Espace Francophone Pneumol, France.
    Kolek, V.
    University Hospital Olomouc, Czech Republic.
    Koppelman, G. H.
    University of Groningen, Netherlands.
    Kowalski, M. L.
    Medical University of Lodz, Poland.
    Kull, I.
    Sachs Childrens Hospital, Sweden; Karolinska Institute, Sweden.
    Kuna, P.
    Medical University of Lodz, Poland.
    Kvedariene, V.
    Vilnius State 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.
    Lipworth, B.
    University of Dundee, Scotland.
    Li, J.
    Guangzhou Medical University, Peoples R China.
    Louis, R.
    CHU Sart Tilman, Belgium.
    Magard, Y.
    Hop St Joseph, France.
    Magnan, A.
    University of Nantes, France.
    Mahboub, B.
    Rashid Hospital, U Arab Emirates.
    Makela, M. J.
    Helsinki University Hospital, Finland.
    De Manuel Keenoy, E.
    Kronikgune, Spain.
    Marshall, G. D.
    University of Mississippi, MS 39216 USA.
    Masjedi, M. R.
    Shahid Beheshti University of Medical Science, Iran.
    Maurer, M.
    Charite, Germany; Charite, Germany.
    Mavale-Manuel, S.
    Maputo Central Hospital, Mozambique.
    Melen, E.
    Karolinska Institute, Sweden.
    Melo-Gomes, E.
    Fac Medical Lisbon, Portugal.
    Meltzer, E. O.
    Allergy and Asthma Medical Grp and Research Centre, CA USA.
    Merk, H.
    Rhein Westfal TH Aachen, Germany.
    Miculinic, N.
    Croatian Pulm Soc, Croatia.
    Mihaltan, F.
    National Institute Pneumol M Nasta, Romania.
    Milenkovic, B.
    University of Belgrade, Serbia; Serbian Assoc Asthma and COPD, Serbia.
    Mohammad, 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.
    Moesges, R.
    University of Cologne, Germany.
    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.
    Neffen, H.
    Hospital Ninos Orlando Alassia, Argentina.
    Nekam, K.
    Hospital Hospitaller Bros Buda, Hungary.
    Niggemann, B.
    Charite, Germany.
    Nyembue, T. D.
    University Hospital Kinshasa, Zaire.
    OHehir, R. E.
    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 Gaulle, Burkina Faso.
    Pali-Schoell, I.
    University of Vienna, Austria; University of Vet Medical Vienna, Austria; University of Vet Medical Vienna, Austria; University of Vienna, Austria.
    Palmer, S.
    University of York, England.
    Panzner, P.
    Charles University of Prague, Czech Republic; .
    Papi, A.
    University of Ferrara, Italy.
    Park, H. S.
    Ajou University, South Korea.
    Pavord, I.
    University of Oxford, England.
    Pawankar, R.
    Nippon Medical Sch, Japan.
    Pfaar, O.
    Centre Rhinol and Allergol, Germany; Heidelberg University, Germany.
    Picard, R.
    Conseil Gen Econ, France.
    Pigearias, B.
    Soc Pneumol Langue Francaise, France; Espace Francophone Pneumol, France.
    Pin, I.
    CHU Grenoble, France.
    Plavec, D.
    University Hospital Pisa, Italy; University of JJ Strossmayer, Croatia.
    Pohl, W.
    Hietzing Hospital, Austria.
    Popov, T. A.
    Medical University of Sofia, Bulgaria.
    Portejoie, F.
    European Innovat Partnership Act and Health Ageing Re, France.
    Postma, D.
    University of Groningen, Netherlands.
    Potter, P.
    University of Cape Town, South Africa.
    Price, D.
    University of Aberdeen, Scotland; Research Real Life, England.
    Rabe, K. F.
    LungenClin Grosshansdorf, Germany; University of Kiel, Germany.
    Raciborski, F.
    Medical University of Warsaw, Poland.
    Radier Pontal, F.
    Maison Profess Liberales, France.
    Repka-Ramirez, S.
    SLAAI, Mexico.
    Robalo-Cordeiro, C.
    Hospital University of Coimbra, Portugal.
    Rolland, C.
    Assoc Asthme and Allergie, France.
    Reitamo, S.
    Helsinki University Hospital, Finland.
    Roman Rodriguez, M.
    Institute Invest Sanitaria Palma IdisPa, Spain.
    Romano, A.
    Complesso Integrato Columbus, Italy.
    Rosario, N.
    University of Federal Parana, Brazil.
    Rosenwasser, L.
    University of Misouri, MI USA.
    Rottem, M.
    Emek Medical Centre, Israel.
    Sanchez-Borges, M.
    Centre Meddocente La, Venezuela; Clin El Avila, Venezuela.
    Scadding, G. K.
    UCL, England.
    Serrano, E.
    CHU Rangueil Larrey, France.
    Schmid-Grendelmeier, P.
    University of Zurich Hospital, Switzerland.
    Sheikh, A.
    University of Edinburgh, Scotland.
    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.
    Euroasian Resp Soc, Kyrgyzstan.
    Spranger, O.
    Global Allergy and Asthma Platform GAAPP, Austria.
    Stelmach, R.
    University of Sao Paulo, Brazil.
    Strandberg, T.
    European Union Geriatr Medical Soc, Austria.
    Sunyer, J.
    Centre Research Environm Epidemiol, Spain; Hospital del Mar, Spain; CIBER Epidemiol and Salud Publ, Spain; University of Pompeu Fabra, Spain.
    Thijs, C.
    Maastricht University, Netherlands.
    Todo-Bom, A.
    University of Coimbra, Portugal.
    Triggiani, M.
    University of Salerno, Italy.
    Valenta, R.
    Medical University of Vienna, Austria.
    Valero, A. L.
    IDIBAPS, Spain.
    van Hage, M.
    Karolinska Institute, Sweden.
    Vandenplas, O.
    Catholic University of Louvain, Belgium.
    Vezzani, G.
    Research Hospital, Italy; Regional Agency Health and Social Care, Italy.
    Vichyanond, P.
    Mahidol University, Thailand.
    Viegi, G.
    CNR, Italy.
    Wagenmann, M.
    University of Klinikum Dusseldorf, Germany.
    Walker, S.
    Asthma UK, England.
    Wang, D. Y.
    National University of Singapore, Singapore.
    Wahn, U.
    Aura Andalucia, Jaen, Spain.
    Williams, D. M.
    University of N Carolina, NC USA.
    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.
    Zar, H. J.
    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.
    Chatzi, L,
    Mercier, J.
    University of Montpellier, France.
    Dedeu, T,
    Hyland, ME,
    Majer, I,
    Manning, P,
    Paggiaro, P,
    Rosado-Pinto, J,
    Rodenas, F,
    MACVIA-ARIA Sentinel NetworK for allergic rhinitis (MASK-rhinitis): the new generation guideline implementation2015Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 70, nr 11, s. 1372-1392Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Several unmet needs have been identified in allergic rhinitis: identification of the time of onset of the pollen season, optimal control of rhinitis and comorbidities, patient stratification, multidisciplinary team for integrated care pathways, innovation in clinical trials and, above all, patient empowerment. MASK-rhinitis (MACVIA-ARIA Sentinel NetworK for allergic rhinitis) is a simple system centred around the patient which was devised to fill many of these gaps using Information and Communications Technology (ICT) tools and a clinical decision support system (CDSS) based on the most widely used guideline in allergic rhinitis and its asthma comorbidity (ARIA 2015 revision). It is one of the implementation systems of Action Plan B3 of the European Innovation Partnership on Active and Healthy Ageing (EIP on AHA). Three tools are used for the electronic monitoring of allergic diseases: a cell phone-based daily visual analogue scale (VAS) assessment of disease control, CARAT (Control of Allergic Rhinitis and Asthma Test) and e-Allergy screening (premedical system of early diagnosis of allergy and asthma based on online tools). These tools are combined with a clinical decision support system (CDSS) and are available in many languages. An e-CRF and an e-learning tool complete MASK. MASK is flexible and other tools can be added. It appears to be an advanced, global and integrated ICT answer for many unmet needs in allergic diseases which will improve policies and standards.

  • 8.
    Bruhn, Sören
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Barrenäs, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Mobini, R.
    Östergötlands Läns Landsting.
    Andersson, B. A.
    Sahlgrenska University Hospital.
    Chavali, S.
    MRC Lab Molecular Biol, Cambridge, UK.
    Egan, B. S.
    Genepathway, Inc., San Diego, CA, USA.
    Hovig, E.
    Norwegian Radium Hospital.
    Sandve, G. K.
    University of Oslo.
    Langston, M. A.
    University of Tennessee, Knoxville, TN, USA.
    Rogers, G.
    University of Tennessee, Knoxville, TN, USA.
    Wang, Hui
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Benson, Mikael
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Increased expression of IRF4 and ETS1 in CD4+ cells from patients with intermittent allergic rhinitis2012Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 67, nr 1, s. 33-40Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The transcription factor (TF) IRF4 is involved in the regulation of Th1, Th2, Th9, and Th17 cells, and animal studies have indicated an important role in allergy. However, IRF4 and its target genes have not been examined in human allergy. Methods: IRF4 and its target genes were examined in allergen-challenged CD4+ cells from patients with IAR, using combined gene expression microarrays and chromatin immunoprecipitation chips (ChIP-chips), computational target prediction, and RNAi knockdowns. Results: IRF4 increased in allergen-challenged CD4+ cells from patients with IAR, and functional studies supported its role in Th2 cell activation. IRF4 ChIP-chip showed that IRF4 regulated a large number of genes relevant to Th cell differentiation. However, neither Th1 nor Th2 cytokines were the direct targets of IRF4. To examine whether IRF4 induced Th2 cytokines via one or more downstream TFs, we combined gene expression microarrays, ChIP-chips, and computational target prediction and found a putative intermediary TF, namely ETS1 in allergen-challenged CD4+ cells from allergic patients. ETS1 increased significantly in allergen-challenged CD4+ cells from patients compared to controls. Gene expression microarrays before and after ETS1 RNAi knockdown showed that ETS1 induced Th2 cytokines as well as disease-related pathways. Conclusions: Increased expression of IRF4 in allergen-challenged CD4+ cells from patients with intermittent allergic rhinitis leads to activation of a complex transcriptional program, including Th2 cytokines.

  • 9.
    Böttcher, Malin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Jenmalm, Maria
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Björkstén, Bengt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Immune responses to birch in young children during their first 7 years of life2002Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 57, s. 43-43Konferensbidrag (Övrigt vetenskapligt)
  • 10.
    Casas, Rosaura
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Ferrándiz, RA
    Wihl, j-Å
    Fernández, B
    Dreborg, S
    Biologic activity of Dermatophagoides siboney and Blomia tropicalis allergens in exposed and unexposed mite-allergic individuals. Effect of patient selection on the biologic standardization of mite extracts.  1999Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 54, s. 392-396Artikel i tidskrift (Refereegranskat)
  • 11.
    Casas, Rosaura
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Jenmalm, Maria
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Björkstén, Bengt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Cat allergen induced cytokine secretion in relation with the detection of Fel d 1-IgG immune complexes in cord blood2002Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 57, s. 135-135Konferensbidrag (Övrigt vetenskapligt)
  • 12. Cortolani, C
    et al.
    Bruijnzeel-Koomen, C
    Bengtsson, U
    Bindslev-Jensen, C
    Björkstén, B
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Höst, AG
    Ispano, Mahfuzar
    Jarish, R
    Madsen, C
    Nekamp, K
    Paganelli, P
    Poulsen, LK
    Wythrich, B
    Controversial aspects of adverse reactions to food. 1999Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 54, s. 27-45Artikel i tidskrift (Refereegranskat)
  • 13.
    Duchen, Karel
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Are human milk polyunsaturated fatty acids (PUFA) related to atopy in the mother and her child?2001Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 56, nr 7, s. 587-592Artikel i tidskrift (Refereegranskat)
  • 14.
    Dzidic, Majda
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. CSIC, Spain; FISABIO, Spain; CIBER ESP, Spain.
    Abrahamsson, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Barn- och kvinnocentrum, H.K.H. Kronprinsessan Victorias barn- och ungdomssjukhus.
    Artacho, A.
    FISABIO, Spain; CIBER ESP, Spain.
    Collado, M. C.
    CSIC, Spain.
    Mira, A.
    FISABIO, Spain; CIBER ESP, Spain.
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Oral microbiota maturation during the first 7 years of life in relation to allergy development2018Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 73, nr 10, s. 2000-2011Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background Allergic diseases have become a major public health problem in affluent societies. Microbial colonization early in life seems to be critical for instructing regulation on immune system maturation and allergy development in children. Even though the oral cavity is the first site of encounter between a majority of foreign antigens and the immune system, the influence of oral bacteria on allergy development has not yet been reported. Objective Methods We sought to determine the bacterial composition in longitudinally collected saliva samples during childhood in relation to allergy development. Illumina sequencing of the 16S rDNA gene was used to characterize the oral bacterial composition in saliva samples collected at 3, 6, 12, 24 months, and 7 years of age from children developing allergic symptoms and sensitization (n = 47) and children staying healthy (n = 33) up to 7 years of age. Results Conclusion Children developing allergic disease, particularly asthma, had lower diversity of salivary bacteria together with highly divergent bacterial composition at 7 years of age, showing a clearly altered oral microbiota in these individuals, likely as a consequence of an impaired immune system during infancy. Moreover, the relative amounts of several bacterial species, including increased abundance of Gemella haemolysans in children developing allergies and Lactobacillus gasseri and L. crispatus in healthy children, were distinctive during early infancy, likely influencing early immune maturation. Early changes in oral microbial composition seem to influence immune maturation and allergy development. Future experiments should test the probiotic potential of L. gasseri and L. crispatus isolates.

  • 15.
    Gawel, Danuta
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    James, A. Rani
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Benson, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Allergicentrum US. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Liljenstrom, R.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Muraro, A.
    Padua University Hospital, Italy .
    Nestor, Colm
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Zhang, Huan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Gustafsson, Mika
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    The Allergic Airway Inflammation Repository - a user-friendly, curated resource of mRNA expression levels in studies of allergic airways2014Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 69, nr 8, s. 1115-1117Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Public microarray databases allow analysis of expression levels of candidate genes in different contexts. However, finding relevant microarray data is complicated by the large number of available studies. We have compiled a user-friendly, open-access database of mRNA microarray experiments relevant to allergic airway inflammation, the Allergic Airway Inflammation Repository (AAIR, http://aair.cimed.ike.liu.se/). The aim is to allow allergy researchers to determine the expression profile of their genes of interest in multiple clinical data sets and several experimental systems quickly and intuitively. AAIR also provides quick links to other relevant information such as experimental protocols, related literature and raw data files.

  • 16.
    Jacobsen, L.
    et al.
    ALK-Abelló, Hørsholm, Denmark.
    Niggemann, B.
    Department of Pediatric Pneumology and Immunology, Charité, Berlin, Germany.
    Dreborg, S.
    Department of Pediatrics, University Hospital of Oslo, Oslo, Norway.
    Ferdousi, Hosne Ara
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Halken, S.
    Department of Pediatrics, Hospital of Sønderborg, Sønderborg, Denmark.
    Høst, A.
    Department of Pediatrics, University Hospital of Odense, Odense, Denmark.
    Koivikko, Antti
    Turku Allergy Centre, Turku, Finland.
    Norberg, L.A.
    Department of Pediatrics, University Hospital of Odense, Odense, Denmark.
    Valovirta, E.
    Turku Allergy Centre, Turku, Finland.
    Wahn, U.
    Department of Pediatric Pneumology and Immunology, Charité, Berlin, Germany.
    Möller, C.
    Department of Pediatrics, Umeå University, Umeå, Sweden.
    Specific immunotherapy has long-term preventive effect of seasonal and perennial asthma: 10-year follow-up on the PAT study2007Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 62, nr 8, s. 943-948Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background:  3-year subcutaneous specific immunotherapy (SIT) in children with seasonal allergic rhinoconjunctivitis reduced the risk of developing asthma during treatment and 2 years after discontinuation of SIT (5-year follow-up) indicating long-term preventive effect of SIT.

    Objective:  We evaluated the long-term clinical effect and the preventive effect of developing asthma 7-years after termination of SIT.

    Methods:  One hundred and forty-seven subjects, aged 16–25 years with grass and/or birch pollen allergy was investigated 10 years after initiation of a 3-year course of SIT with standardized allergen extracts of grass and/or birch or no SIT respectively. Conjunctival provocations were performed outside the season and methacholine bronchial provocations were performed during the season and winter. Asthma was assessed by clinical evaluation.

    Results:  The significant improvements in rhinoconjunctivitis and conjunctival sensitivity persisted at the 10-year follow-up. Significantly less actively treated subjects had developed asthma at 10-year follow-up as evaluated by clinical symptoms [odds ratio 2.5 (1.1–5.9)]. Patients who developed asthma among controls were 24/53 and in the SIT group 16/64. The longitudinal treatment effect when adjusted for bronchial hyper-responsiveness and asthma status at baseline including all observations at 3, 5 and 10 years follow-up (children with or without asthma at baseline, n = 189; 511 observations) was statistically significant (P = 0.0075). The odds ratio for no-asthma was 4.6 95% CI (1.5–13.7) in favor of SIT.

    Conclusion:  A 3-year course of SIT with standardized allergen extracts has shown long-term clinical effects and the potential of preventing development of asthma in children with allergic rhinoconjunctivitis up to 7 years after treatment.

    Clinical implication:  Specific immunotherapy has long-term clinical effects and the potential of preventing development of asthma in children with allergic rhino conjunctivitis up to 7 years after treatment termination.

  • 17.
    Janefjord, Camilla
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Aniansson-Zdolsek, H
    Jenmalm, Maria
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Reduced IL-12 receptor beta 2 up-regulation after IL-2 and IL-12 stimulation in atopic children2002Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 57, s. 129-129Konferensbidrag (Övrigt vetenskapligt)
  • 18.
    Johansson, S.
    et al.
    Department of Pediatrics, Göteborg University, Queen Silvia Children's Hospital, Sweden.
    Keen, C.
    Department of Pediatrics, Göteborg University, Queen Silvia Children's Hospital, Sweden.
    Ståhl, A.
    , Göteborg University, Sahlgrenska Hospital, Göteborg, Sweden.
    Wennergren, G.
    Department of Pediatrics, Göteborg University, Queen Silvia Children's Hospital, Sweden.
    Benson, Mikael
    Department of Pediatrics, Göteborg University, Queen Silvia Children's Hospital, Sweden.
    Low levels of CC16 in nasal fluid of children with birch pollen-induced rhinitis2005Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 60, nr 5, s. 638-642Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background:  Clara cell protein 16 (CC16; secretoglobin 1A1) is an anti-inflammatory protein mainly expressed in the epithelial cells in the airways.

    Objective:  To compare the levels of CC16 in nasal lavage (NAL) from children with intermittent allergic rhinitis and healthy controls and to study the effect of a local steroid.

    Methods:  Thirty schoolchildren with birch pollen allergy and 30 healthy controls from the same schools were included in the study. The NAL fluid was collected before the season, during the birch pollen season and, for the patients, after 1 week of treatment with a local steroid. Symptom scores were obtained on every occasion. CC16 and eosinophil cationic protein (ECP) were analyzed with enzyme-linked immunosorbent assay.

    Results:  The nasal fluid levels of CC16 were significantly lower in patients than in controls, before and during pollen season. Before the season, the median CC16 concentrations were 9.1 (range 1.1–117) μg/l in patients and 25.7 (6.1–110.2) μg/l in controls. During the season, the median CC16 concentrations in nasal fluid were 12.9 (2.3–89.7) μg/l in the allergic children and 22.0 (9.5–90.1) μg/l in the healthy controls (P = 0.0005). Symptom scores, nasal fluid eosinophils and ECP were higher in patients during the season. Treatment with a local steroid did not change the CC16 levels.

    Conclusions:  Nasal fluid CC16 levels were lower in children with birch pollen-induced allergic rhinitis than in healthy controls both before and during the pollen season. We speculate that reduction in anti-inflammatory activity by CC16 may contribute to the pathogenesis of allergic rhinitis.

  • 19. Lindstrom, AK
    et al.
    Böttcher, Malin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Polymorphism of the CD14 gene in relation to atopic disease2002Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 57, s. 214-214Konferensbidrag (Övrigt vetenskapligt)
  • 20.
    Mai, Xiaomei
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik.
    Fagerås Böttcher, Malin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik.
    Bruhammar, M
    Allergicentrum US, Linköping.
    Nilsson, Lennart
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Zetterström, Olle
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Allergicentrum. Östergötlands Läns Landsting, Medicincentrum, Allergicentrum US.
    Urinary inflammatory mediators and inhalation of hypertonic saline in children2005Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 60, nr 1, s. 60-64Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The inflammatory mechanisms of hypertonic saline-induced bronchoconstriction are not well understood. Methods: Seventeen asthmatics with (n = 11) and without bronchial hyperresponsiveness (BHR) (n = 6) and 18 randomly selected nonatopic nonasthmatic controls without BHR were evaluated by urine samples collected before and 1 h after hypertonic saline provocation test. Histamine, 11β-PGF2α, and LTE4 were analysed by enzyme immunoassay (EIA) and eosinophil protein X (EPX) by radioimmunoassay (RIA). Results: The levels of leukotriene E4 (LTE4) increased significantly after the challenge tests, both in the asthmatics (median: 354 pg/mg pre-challenge vs. 628 pg/mg post-challenge, P = 0.05) and in the controls (median: 294 pg/mg pre-challenge vs. 460 pg/mg post-challenge, P < 0.01). The levels of histamine also increased significantly in the latter (median: 299 μmol/mg pre-challenge vs. 569 μmol/mg post-challenge, P = 0.03). However, the levels of 11β-PGF2α and EPX did not change significantly after the challenge tests either in the asthmatics or in the controls. Conclusions: The inhalation of hypertonic saline increased urinary excretion of LTE4 both in the asthmatics and in the controls. The slight increase of leukotrienes was enough to induce airway obstruction in some of the asthmatics, because of the hyperresponsiveness in their airways.

  • 21.
    Nestor, Colm E
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Dadfa, Elham
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Ernerudh, Jan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för inflammationsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Diagnostikcentrum, Klinisk immunologi och transfusionsmedicin.
    Gustafsson, Mika
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Björkander, Jan Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för inflammationsmedicin. Linköpings universitet, Hälsouniversitetet.
    Benson, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Allergicentrum US. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Zhang, Huan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Sublingual immunotherapy alters expression of IL-4 and its soluble and membrane-bound receptors2014Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 69, nr 11, s. 1564-1566Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Seasonal allergic rhinitis (SAR) is a disease of increasing prevalence, which results from an inappropriate T-helper cell, type 2 (Th2) response to pollen. Specific immunotherapy (SIT) involves repeated treatment with small doses of pollen and can result in complete and lasting reversal of SAR. Here, we assayed the key Th2 cytokine, IL-4, and its soluble and membrane-bound receptor in SAR patients before and after SIT. Using allergen-challenge assays, we found that SIT treatment decreased IL-4 cytokine levels, as previously reported. We also observed a significant decrease in the IL-4 membrane-bound receptor (mIL4R) at both the level of mRNA and protein. SIT treatment resulted in a significant increase in the inhibitory soluble IL-4 receptor (sIL4R). Reciprocal changes in mIL4R and sIL4R were also observed in patient serum. Altered mIL4R and sIL4R is a novel explanation for the positive effects of immunotherapy with potential basic and clinical research implications.

  • 22.
    Niggemann, B.
    et al.
    Department of Pediatric Pneumology and Immunology, Charité, Berlin, Germany, Department of Pediatric Pneumology and Immunology, University Children's Hospital Charité, Augustenburger Platz 1, 13353 Berlin, Germany.
    Jacobsen, L.
    ALK-Abelló, Hørsholm, Denmark.
    Dreborg, S.
    Department of Pediatrics, University Hospital of Oslo, Oslo, Norway.
    Ferdousi, Hosne Ara
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Halken, S.
    Department of Pediatrics, Hospital of Sønderborg, Sønderborg, Denmark.
    Høst, A.
    Department of Pediatrics, University Hospital of Odense, Odense, Denmark.
    Koivikko, A.
    Turku Allergy Centre, Turku, Finland.
    Koller, D.
    Department of Pediatrics, University Hospital Vienna, Vienna, Austria.
    Norberg, L.A.
    Department of Pediatrics, University Hospital of Odense, Odense, Denmark.
    Urbanek, R.
    Department of Pediatrics, University Hospital Vienna, Vienna, Austria.
    Valovirta, E.
    Turku Allergy Centre, Turku, Finland.
    Wahn, U.
    Department of Pediatric Pneumology and Immunology, Charité, Berlin, Germany.
    Möller, C.
    Department of Pediatrics, Umeå University, Umeå, Sweden.
    Five-year follow-up on the PAT study: specific immunotherapy and long-term prevention of asthma in children2006Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 61, nr 7, s. 855-859Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background:  A 3-year course of specific immunotherapy (SIT) in children with hay fever to grass and/or birch pollen significantly reduced the risk of developing asthma. To investigate the long-term preventive effect, we performed a follow up – 2 years after termination of immunotherapy.

    Methods:  A total of 183 children, aged 6–14 years with grass and/or birch pollen allergy could be investigated 2 years after discontinuation of SIT or no treatment. Conjunctival provocation tests (CPTs) and methacholine bronchial provocation tests were carried out during the season and winter after 5 years. The development of asthma was assessed by clinical evaluation.

    Results:  The significant improvement in hay fever and CPT results observed after 3 years of SIT persisted at the 5-year follow-up. No difference in bronchial responsiveness to methacholine was found after 5 years because of spontaneous improvement during the follow-up period in the control patients. The immunotherapy-treated children had significantly less asthma after 5 years as evaluated by clinical symptoms [odds ratio 2.68 (1.3–5.7)] in favor of SIT for prevention of development of asthma and significantly less patients reported an increase in asthma scores (P < 0.01).

    Conclusion:  Immunotherapy for 3 years with standardized allergen extracts of grass and/or birch shows long-term clinical effect and preventive effect on development of asthma in children with seasonal rhinoconjunctivitis.

  • 23.
    Nilsson, Lennart
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Castor, O
    Löfman, O
    Magnusson, A
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Yrkes- och miljömedicin. Östergötlands Läns Landsting, Smärt- och yrkesmedicinskt centrum, Yrkes- och miljömedicinskt centrum.
    Kjellman, Max
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Allergic disease in teenagers in relation to urban or rural residence at various stages of childhood.  1999Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 54, s. 716-721Artikel i tidskrift (Refereegranskat)
  • 24.
    Nopp, A
    et al.
    Dept of Medicine KI, Stockholm.
    Johansson, SGO
    Dept of Medicine KI, Stockholm.
    Ankerst, J
    Dept of Medicine, Lund.
    Bylin, G
    Dept of Medicine Karolinska Hosp, Huddinge.
    Cardell, LO
    Lab Exp Allergy Res, Malmö University Hospital.
    Grönneberg, R
    Dept of Respiratory Medicine Karolinska Hospital, Stockholm.
    Irander, Kristina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik.
    Palmqvist, M
    The Lung Pharmacology Group, Sahlgrenska University Hospital.
    Öman, H
    MIAB, Uppsala.
    Basophil allergen threshold sensitivity: A useful approach to anti-IgE treatment efficacy evaluation2006Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 61, nr 3, s. 298-302Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Monitoring of the allergen sensitivity of a patient is most important for optimal patient care and a basic prerequisite for immunomodulating treatment. The objective of this study was to investigate how basophil allergen sensitivity can be applied in the monitoring of anti-immunoglobulin E (IgE) treatment. Methods: Basophils from timothy grass pollen allergic patients were, by flow cytometry, analysed for allergen threshold sensitivity (CD-sens) by measuring CD63 up-regulation on CD203c-identified basophils. The results were compared with maximal percentage CD63 up-regulation at one allergen dose (CD-max), skin prick test end-point allergen titration, (SPT-sens), nasal provocation titration tests (nasal provocation titre) and serum IgE and IgE antibody concentrations. Results: There was a significant correlation (r = 0.50, P = 0.01) between CD-sens and SPT-sens, CD-sens and the IgE antibody concentration in percentage of 'total IgE' (relative IgE antibody concentration) (r = 0.72, P < 0.001) as well as between CD-sens and nasal provocation titre (r = 0.54, P < 0.05) but, in contrast, CD-max did not correlate with any of the sensitization parameters, i.e. SPT-sens, nasal provocation titre, absolute and relative IgE antibody concentration or CD-sens. CD-sens could be used to monitor omalizumab treatment efficacy while, based on CD-max, four of seven symptom-free patients on omalizumab would have been classified as having ongoing allergy. Conclusions: CD-sens seems to be very useful for the determination of a patient's allergen sensitivity and should be evaluated for the measurement and monitoring of anti-IgE treatment efficacy. CD-max, the conventional approach to basophil allergen challenge, which mirrors cell reactivity, gives incorrect information. Copyright © Blackwell Munksgaard 2006.

  • 25. Oldeaus, G
    et al.
    Björkstén, B
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Jenmalm, Maria
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Kjellman, Max
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Cow's milk IgE and IgG antibody responses to cow's milk formulas. 1999Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 54, s. 352-357Artikel i tidskrift (Refereegranskat)
  • 26.
    Olsson, M.
    et al.
    Department of Pediatrics, Queen Silvia Children's Hospital, Gothenburg, Sweden.
    Broberg, A.
    Department of Dermatology, Sahlgrenska Academy, Gothenburg, Sweden.
    Jernås, M.
    Research Centre for Endocrinology and Metabolism, Sahlgrenska Academy, Gothenburg, Sweden.
    Carlsson, L.
    Research Centre for Endocrinology and Metabolism, Sahlgrenska Academy, Gothenburg, Sweden.
    Rudemo, M.
    Department of Mathematical Statistics, Chalmers University of Technology, Gothenburg, Sweden.
    Suurküla, M.
    Department of Pathology, Sahlgrenska Academy, Gothenburg, Sweden.
    Svensson, P-A
    Research Centre for Endocrinology and Metabolism, Sahlgrenska Academy, Gothenburg, Sweden.
    Benson, Mikael
    Department of Pediatrics, Queen Silvia Children's Hospital, Gothenburg, Sweden.
    Increased expression of aquaporin 3 in atopic eczema2006Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 61, nr 9, s. 1132-1137Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Dry skin in atopic eczema depends on increased water loss. The mechanisms behind this are poorly understood. The aim of this work was to identify genes that may contribute to water loss in eczema.

    METHODS: Affymetrix DNA microarrays U133A were used to analyse gene expression in skin biopsies from 10 patients with atopic eczema and 10 healthy controls.

    RESULTS: DNA microarray analysis showed up-regulation of 262 genes and down-regulation of 129 genes in atopic eczema. The known functions of these genes were analysed using Gene Ontology to identify genes that could contribute to increased water loss. This led to identification of aquaporin 3 (AQP3), which has a key role in hydrating healthy epidermis. Increased expression of AQP3 was found in eczema compared with healthy skin. This was confirmed with real-time polymerase chain reaction (P<0.001). In healthy skin, epidermal AQP3 immunoreactivity was weak and mainly found in the stratum basale. A gradient was formed with decreasing AQP3 staining in the lower layers of the stratum spinosum. By contrast, in acute and chronic atopic eczema strong AQP3 staining was found in both the stratum basale and the stratum spinosum.

    CONCLUSIONS: Aquaporin 3 is the predominant aquaporin in human skin. Increased expression and altered cellular distribution of AQP3 is found in eczema and this may contribute to water loss.

  • 27. Prescott, SL
    et al.
    Holt, PG
    Jenmalm, Maria
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik.
    Björkstén, Bengt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Effects of maternal allergen-specific IgG in cord blood on early postnatal development of allergen-specific T-cell immunity2000Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 55, nr 5, s. 470-475Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: A wide body of epidemiologic evidence indicates that as yet unknown maternal factor(s) can influence susceptibility to allergic disease in the offspring. It is also well established that the induction of allergen- specific T-cell memory is frequently initiated in utero, and it is likely that maternal factors exert their influence during this period. Methods: This study examines the relationship between maternally derived allergen-specific IgG subclass antibodies and cellular immune responses (lymphoproliferation and cytokine production) against the same allergens in 49 subjects tested at birth and at 2 years of age. Polyclonal production of the Th1 cytokine IFN-? was also examined in the cord-blood samples. Results: At birth, there were positive correlations between both house-dust mite (HDM)- and ovalbumin (OVA)-specific IgG subclass levels in cord blood, maternal atopy, and the magnitude of perinatal lymphoproliferative responses to respective allergens. Inverse relationships were also observed between cord-blood IgG antibody titres and allergen-specific production of some Th2 cytokines. However, there were no consistent relationships between cord-blood allergen-specific IgG antibodies and subsequent immune responses to allergens when the same subjects were retested at 2 years of age. An inverse relationship was observed between maternal history of atopy and perinatal IFN-Ac production capacity. Conclusions: Our results suggest that transplacental transfer of allergen-specific IgG antibody is unlikely to be a major mechanism for maternal regulation of allergen-specific immunity in infancy. An alternative possibility is that maternal effects may operate by influencing IFN-? production by T cells in the offspring.

  • 28.
    Protudjer, Jennifer L. P.
    et al.
    Karolinska Inst, Sweden; Karolinska Inst, Sweden; Univ Manitoba, Canada; George and Fay Yee Ctr Healthcare Innovat, Canada; Childrens Hosp Res Inst Manitoba, Canada.
    Middelveld, Roelinde
    Karolinska Inst, Sweden.
    Ballardini, Natalia
    Karolinska Inst, Sweden; Soder Sjukhuset, Sweden; Kings Coll London, England.
    Wai, Hay Mar
    Karolinska Inst, Sweden.
    Ahlstedt, Staffan
    Karolinska Inst, Sweden.
    Nilsson, Lennart E
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi, infektion och inflammation. Linköpings universitet, Medicinska fakulteten.
    Kivisto, Juho E.
    Tampere Univ Hosp, Finland; Univ Tampere, Finland.
    Epinephrine dispensings, allergy hospitalizations and the elimination of co-payments in Sweden2019Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 74, nr 6, s. 1197-1200Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    n/a

  • 29.
    Ringsberg, K
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för hälsa och samhälle, Socialmedicin och folkhälsovetenskap.
    Timpka, Toomas
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för hälsa och samhälle, Socialmedicin och folkhälsovetenskap. Östergötlands Läns Landsting, Folkhälsovetenskapligt centrum, Folkhälsovetenskapligt centrum.
    Clinical health education for patients with asthma-like symptoms but negative asthma tests2001Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 56, nr 11, s. 1049-1054Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Patients with asthma-like symptoms but negative asthma tests often state that they lack strategies to cope with their symptoms. The aim of the study was to determine whether a problem-based health education program had a beneficial effect on the participants' experience of symptoms and subjective health. Methods: Thirty-eight patients, consecutively drawn from an outpatient clinic for asthma and allergy, were randomly allocated to an intervention group (I group, n = 18) and a control group (C group, n = 20). The I group, divided into three subgroups, met on seven occasions over 5 months. The program had a multidisciplinary approach, used exercises inspired by cognitive behavioral therapy, and was performed according to the principles of problem-based learning. All patients answered the Nijmegen Symptom Questionnaire (NQ) and the SF-36 health survey before and 2 months after the training was terminated. Results: Before the program, there were no significant differences between the groups in their earlier experience of symptoms. After it, the I group scored significantly lower on shortness of breath (P = 0.001) and central tetany (P = 0.05) than the C group. On both test occasions, the asthma-like patients scored lower on all variables of the SF-36 than the reference groups of asthmatics and healthy subjects. No significant differences were seen between the I group and the C group except for vitality, in which the C group scored lower before the intervention. Conclusions: Patients with asthma-like symptoms but negative asthma tests benefit from taking part in a problem-based health education program. It mainly reduces the frequency of symptoms.

  • 30.
    Sjogren, A-K M
    et al.
    University of Gothenburg.
    Barrenäs, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Muraro, A
    Padua Gen University Hospital.
    Gustafsson, Mika
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Saetrom, P
    University of Gothenburg.
    Wang, Hui
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Benson, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Monozygotic twins discordant for intermittent allergic rhinitis differ in mRNA and protein levels2012Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 67, nr 6, s. 831-833Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Monozygotic (MZ) twins discordant for complex diseases may help to find disease mechanisms that are not due to genetic variants. Intermittent allergic rhinitis (IAR) is an optimal disease model because it occurs at defined time points each year, owing to known external antigens. We hypothesized that MZ twins discordant for IAR could help to find gene expression differences that are not dependent on genetic variants. We collected blood outside of the season from MZ twins discordant for IAR, challenged their peripheral blood mononuclear cells (PBMC) with pollen allergen in vitro, collected supernatants and isolated CD4+ T cells. We identified disease-relevant mRNAs and proteins that differed between the discordant MZ twins. By contrast, no differences in microRNA expression were found. Our results indicate that MZ twins discordant for IAR is an optimal model to identify disease mechanisms that are not due to genetic variants.

  • 31.
    Toll, Johan B
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Farmakologi.
    Andersson, Rolf G
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Farmakologi.
    Effects of enprofylline and theophylline on purified human basophils1984Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 39, nr 7, s. 515-520Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Extracts from purified human basophils revealed activity of cAMP-phosphodiesterase with a km-value of 0.59 microM. The enzyme was not activated by Ca-ions. Enprofylline and theophylline inhibited the enzyme in a competitive manner. Enprofylline was more potent than theophylline. These drugs did also inhibit the anti-IgE-induced histamine release from the basophils. These results favour the hypothesis that inhibition of histamine release of enprofylline is caused by an inhibition of phosphodiesterase. Although accumulating data have indicated that theophylline, at therapeutic concentrations, is a weak inhibitor of cAMP-phosphodiesterase activity, there is reason to believe that enprofylline, at therapeutic concentrations, may act at least partly as a phosphodiesterase inhibitor.

  • 32.
    Toll, Johan B
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Farmakologi.
    Wikberg, J E
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Farmakologi.
    Andersson, Rolf G
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Farmakologi.
    Purification of human basophils by affinity chromatography on anti-IgE-sepharose 6MB1981Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 36, nr 6, s. 411-417Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    This work describes a method for the purification of basophil leukocytes from human peripheral blood by the use of a three-step separation technique including affinity chromatography on anti-IgE-sepharose 6MB. The purity of the obtained basophils was 50--95% and the recovery was 30--40%. The basophils separated by this method appeared normal and were found to be reactive with anti-IgE in subsequent tests.

  • 33.
    Wang, Hui
    et al.
    University of Gothenburg, Sweden.
    Chavali, S.
    University of Gothenburg, Sweden.
    Mobini, R.
    University of Gothenburg, Sweden.
    Muraro, A.
    University of Padua, Italy.
    Barbon, F.
    University of Padua, Italy.
    Boldrin, D.
    University of Padua, Italy.
    Aberg, N.
    The Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Benson, Mikael
    The Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    A pathway-based approach to find novel markers of local glucocorticoid treatment in intermittent allergic rhinitis2011Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 66, nr 1, s. 132-140Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Glucocorticoids (GCs) may affect the expression of hundreds of genes in different cells and tissues from patients with intermittent allergic rhinitis (IAR). It is a formidable challenge to understand these complex changes by studying individual genes. In this study, we aimed to identify (i) pathways affected by local GC treatment and (ii) examine if those pathways could be used to find novel markers of local GC treatment in nasal fluids from patients with IAR. METHODS: Gene expression microarray- and iTRAQ-based proteomic analyses of nasal fluids, nasal fluid cells and nasal mucosa from patients with IAR were performed to find pathways enriched for differentially expressed genes and proteins. Proteins representing those pathways were analyzed with ELISA in an independent material of nasal fluids from 23 patients with IAR before and after treatment with a local GC. RESULTS: Transcriptomal and proteomic high-throughput analyses of nasal fluids, nasal fluid cells and nasal mucosal showed that local GC treatment affected a wide variety of pathways in IAR such as the glucocorticoid receptor pathway and the acute phase response pathway. Extracellular proteins encoded by genes in those pathways were analyzed in an independent material of nasal fluids from patients. Proteins that changed significantly in expression included known biomarkers such as eosinophil cationic protein but also proteins that had not been previously described in IAR, namely CCL2, M-CSF, CXCL6 and apoH. CONCLUSION: Pathway-based analyses of genomic and proteomic high-throughput data can be used as a complementary approach to identify novel potential markers of GC treatment in IAR.

  • 34. Warner, A
    et al.
    Boström, S
    Möller, C
    Kjellman, Max
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Mite fauna in the home and sensitivity to house-dust and storage mites. 1999Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 54, s. 681-690Artikel i tidskrift (Refereegranskat)
  • 35. Welinder, H
    et al.
    Nielsen, J
    Rylander, L
    Ståhlbom, Bengt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Yrkes- och miljömedicin. Östergötlands Läns Landsting, Smärt- och yrkesmedicinskt centrum, Yrkes- och miljömedicinskt centrum.
    A prospective study of the relationship between exposure and specific antibodies in workers exposed to organic acid anhydrides2001Ingår i: Allergy. European Journal of Allergy and Clinical Immunology, ISSN 0105-4538, E-ISSN 1398-9995, Vol. 56, nr 6, s. 506-511Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The exposure-response relationships for the induction of specific IgE and IgG were evaluated in a prospective study of workers exposed to organic acid anhydrides (OAAs). Special attention was paid to the modifying effects of atopy and smoking. Methods: The subjects were 163 previously unexposed persons exposed to epoxy resins with hexahydro-, methylhexahydro-, and methyltetrahydrophthalic anhydride as curing agents. The levels of OAAs in air and of specific IgE and IgG in serum were recurrently monitored. The mean observation time was 32 (1-105) months. Results: The mean combined OAA exposure of the subjects was 15.4 (< 1-189) ╡g/m3. Positive specific IgE was demonstrated by 21 (13%) subjects with a mean induction time of 8.8 (1-35) months. The incidence of sensitization was 4.1 cases/1000 months at risk. The relative risk (OR) for atopics was 5.4 (1.9-15.3, 95% CI). An exposure-response relationship was demonstrated by an increasing risk of sensitization with increasing exposure. Conclusions: An association between exposure and atopy, respectively, and the induction of specific antibodies against OAAs were observed. The risk for atopics was comparable with the risk for the subjects in the most exposed group.

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