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  • 1.
    Abrahamsson, Thomas
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Jakobsson, Hedvig E.
    Karolinska Institute, Sweden .
    Andersson, Anders F.
    KTH Royal Institute Technology, Sweden .
    Bjorksten, Bengt
    University of Örebro, Sweden .
    Engstrand, Lars
    KTH Royal Institute Technology, Sweden .
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Reply: Gut microbiota diversity and atopic disease: Does breast-feeding play a role?2013Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 131, nr 1, s. 248-249Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    n/a

  • 2.
    Abrahamsson, Thomas
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Jakobsson, Hedvig E
    Department of Preparedness, Swedish Institute for Communicable Disease Control, Solna, Sweden.
    Andersson, Anders F
    Science for Life Laboratory, School of Biotechnology, KTH Royal Institute of Technology, Stockholm, Sweden.
    Björksten, Bengt
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, and the School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Engstrand, Lars
    Department of Preparedness, Swedish Institute for Communicable Disease Control, Solna, Sweden.
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Low diversity of the gut microbiota in infants with atopic eczema2012Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 129, nr 2, s. 434-440Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    It is debated whether a low total diversity of the gut microbiota in early childhood is more important than an altered prevalence of particular bacterial species for the increasing incidence of allergic disease. The advent of powerful, cultivation-free molecular methods makes it possible to characterize the total microbiome down to the genus level in large cohorts.

    Objective

    We sought to assess microbial diversity and characterize the dominant bacteria in stool during the first year of life in relation to atopic eczema development.

    Methods

    Microbial diversity and composition were analyzed with barcoded 16S rDNA 454-pyrosequencing in stool samples at 1 week, 1 month, and 12 months of age in 20 infants with IgE-associated eczema and 20 infants without any allergic manifestation until 2 years of age (ClinicalTrials.gov ID NCT01285830).

    Results

    Infants with IgE-associated eczema had a lower diversity of the total microbiota at 1 month (P = .004) and a lower diversity of the bacterial phylum Bacteroidetes and the genus Bacteroides at 1 month (P = .02 and P = .01) and the phylum Proteobacteria at 12 months of age (P = .02). The microbiota was less uniform at 1 month than at 12 months of age, with a high interindividual variability. At 12 months, when the microbiota had stabilized, Proteobacteria, comprising gram-negative organisms, were more abundant in infants without allergic manifestation (Empirical Analysis of Digital Gene Expression in R [edgeR] test: P = .008, q = 0.02).

    Conclusion

    Low intestinal microbial diversity during the first month of life was associated with subsequent atopic eczema.

  • 3.
    Abrahamsson, Thomas R
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomsmedicinska kliniken US.
    Jakobsson, Ted
    Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomsmedicinska kliniken US.
    Böttcher, Malin Fagerås
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Fredrikson, Mats
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Yrkes- och miljömedicin. Linköpings universitet, Hälsouniversitetet.
    Jenmalm, Maria C
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Björkstén, Bengt
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomsmedicinska kliniken US.
    Oldaeus, Göran
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Probiotics in prevention of IgE-associated eczema: a double-blind, randomized, placebo-controlled trial2007Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 119, nr 5, s. 1174-1180Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: An altered microbial exposure may underlie the increase of allergic diseases in affluent societies. Probiotics may alleviate and even prevent eczema in infants.

    OBJECTIVE: To prevent eczema and sensitization in infants with a family history of allergic disease by oral supplementation with the probiotic Lactobacillus reuteri.

    METHODS: Double-blind, randomized, placebo-controlled trial, which comprised 232 families with allergic disease, of whom 188 completed the study. The mothers received L reuteri ATCC 55730 (1 x 10(8) colony forming units) daily from gestational week 36 until delivery. Their babies then continued with the same product from birth until 12 months of age and were followed up for another year. Primary outcome was allergic disease, with or without positive skin prick test or circulating IgE to food allergens.

    RESULTS: The cumulative incidence of eczema was similar, 36% in the treated versus 34% in the placebo group. The L reuteri group had less IgE-associated eczema during the second year, 8% versus 20% (P = .02), however. Skin prick test reactivity was also less common in the treated than in the placebo group, significantly so for infants with mothers with allergies, 14% versus 31% (P = .02). Wheeze and other potentially allergic diseases were not affected.

    CONCLUSION: Although a preventive effect of probiotics on infant eczema was not confirmed, the treated infants had less IgE-associated eczema at 2 years of age and therefore possibly run a reduced risk to develop later respiratory allergic disease. CLINICAL IMPLICATION: Probiotics may reduce the incidence of IgE-associated eczema in infancy.

  • 4.
    Benson, Mikael
    et al.
    Malmö University Hospital, Sweden.
    Carlsson, Lena
    Sahlgrenska University Hospital, Gothenburg, Sweden.
    Adner, Mikael
    Malmö University Hospital, Sweden.
    Jernås, Margareta
    Sahlgrenska University Hospital, Gothenburg, Sweden.
    Rudemo, Mats
    Chalmers University of Technology, Gothenburg, Sweden.
    Sjögren, Anders
    Chalmers University of Technology, Gothenburg, Sweden.
    Svensson, Per Arne
    Sahlgrenska University Hospital, Gothenburg, Sweden.
    Uddman, Rolf
    Malmö University Hospital, Sweden.
    Cardell, Lars Olaf
    Malmö University Hospital, Sweden.
    Gene profiling reveals increased expression of uteroglobin and other anti-inflammatory genes in glucocorticoid-treated nasal polyps2004Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 113, nr 6, s. 1137-1143Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Treatment with local glucocorticoids (GCs) decreases symptoms and the size of nasal polyps. This might depend on the downregulation of proinflammatory genes, as well as the upregulation of anti-inflammatory genes.

    OBJECTIVE: We sought to identify GC-regulated anti-inflammatory genes in nasal polyps.

    METHODS: Affymetrix DNA microarrays were used to analyze the expression of 22,283 genes in 4 nasal polyps before and after local treatment with fluticasone (400 microg/d). Expression of uteroglobin and mammaglobin B was analyzed with real-time PCR in 6 nasal polyps and in nasal biopsy specimens from 6 healthy control subjects.

    RESULTS: Two hundred three genes had changed in expression in treated polyps, and 139 had known functions: 54 genes were downregulated, and 85 were upregulated. Genes associated with inflammation constituted the largest single functional group. These genes affected key steps in inflammation (eg, immunoglobulin production; antigen processing and presentation; and the chemoattraction and activation of granulocytes, T cells, and B cells). Several proinflammatory genes were downregulated. In contrast, some anti-inflammatory genes were upregulated. The gene that increased most in terms of expression was uteroglobin. This was confirmed with real-time PCR. By contrast, expression of uteroglobin was lower in untreated polyps than in healthy nasal mucosa. Immunohistochemical investigation showed staining of uteroglobin in the epithelium and in seromucous glands in control subjects and in nasal polyps.

    CONCLUSION: Upregulation of anti-inflammatory genes, such as uteroglobin, might contribute to the effects of local treatment with GCs in nasal polyps.

  • 5.
    Benson, Mikael
    et al.
    Department of Pediatrics, Queen Silvia Children's Hospital, Gothenburg, Sweden.
    Langston, Michael A.
    Department of Computer Science, University of Tennessee, Knoxville, USA.
    Adner, Mikael
    Laboratory for Clinical and Experimental Allergy Research, Department of Oto-Rhino-Laryngology, Malmö University Hospital, Lund University, Malmö, Sweden.
    Andersson, Bengt
    Department of Clinical Immunology, Sahlgrenska Academy, Gothenburg, Sweden.
    Torinssson-Naluai, Åsa
    Department of Clinical Genetics and Göteborg Genomics, Sahlgrenska Academy, Gothenburg, Sweden.
    Cardell, Lars Olaf
    Laboratory for Clinical and Experimental Allergy Research, Department of Oto-Rhino-Laryngology, Malmö University Hospital, Lund University, Malmö, Sweden.
    A network-based analysis of the late-phase reaction of the skin2006Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 118, nr 1, s. 220-225Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    The late-phase reaction (LPR) of the skin is an in vivo model of allergic inflammation.

    Objective

    We sought to identify disease-associated pathways in the LPR using a network-based analysis.

    Methods

    The LPR was examined by means of DNA microarray analysis of skin biopsy specimens from 10 patients with allergic rhinitis and 10 healthy control subjects. The results were further analyzed in 2 different materials consisting of nasal fluids and allergen-challenged CD4+ T cells from patients with allergic rhinitis.

    Results

    The DNA microarray analysis revealed several genes of known relevance to allergy. The eosinophil marker Charcot-Leyden crystal protein (CLC) that encodes Charcot-Leyden crystal protein differed most in expression. A network-based analysis showed upregulation of IL-4– and CCL4-dependent pathways and downregulation of a TGF-β–induced pathway. CCL4 is expressed by CD4+ T cells and chemotactic for eosinophils. We hypothesized that allergen induces release of CCL4 from TH2 cells and that this contributes to influx of eosinophils. Further analysis showed increase of CCL4 protein in nasal fluids from allergic patients during the season. Allergen challenge of PBMCs resulted in proliferation of TH2 cells and increased production of CCL4 in CD4+ T cells from allergic patients. An analysis of the DNA microarray data revealed a significant correlation between CCL4 and the eosinophil marker CLC.

    Conclusion

    A network-based analysis of the LPR showed increased activity of IL-4– and CCL4- dependent pathways and downregulation of the TGF-β–induced pathway. Allergen-induced release of CCL4 from TH2 cells might contribute to influx of eosinophils during the LPR.

    Clinical implications

    Involvement of multiple interacting pathways indicates that it might be difficult to identify one single mediator as a biomarker or drug target in allergic inflammation.

  • 6.
    Benson, Mikael
    et al.
    Sahlgrenska University Hospital, Göteborg.
    Strannegård, Inga-Lisa
    Sahlgrenska University Hospital, Göteborg.
    Strannegård, Örjan
    Sahlgrenska University Hospital, Göteborg.
    Wennergren, Göran
    Sahlgrenska University Hospital, Göteborg.
    Topical steroid treatment of allergic rhinitis decreases nasal fluid TH2 cytokines, eosinophils, eosinophil cationic protein, and IgE but has no significant effect on IFN-gamma, IL-1beta, TNF-alpha, or neutrophils2000Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 106, nr 2, s. 307-312Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Topical treatment with glucocorticoids (GCs) is known to decrease eosinophils but not neutrophils in patients with allergic rhinitis.

    OBJECTIVE: We sought to examine whether the differential effects of GC treatment on eosinophils and neutrophils are mirrored by differential effects on T(H)1/T(H)2 cytokines and the neutrophil-associated cytokines IL-1beta and TNF-alpha.

    METHODS: Differential counts of eosinophils and neutrophils in nasal fluids from 60 children with seasonal allergic rhinitis treated with a topical GC were examined after staining with May-Grünwald-Giemsa stain. Nasal fluid levels of IFN-gamma, IL-4, IL-6, IL-10, IL-1beta, and TNF-alpha were examined with ELISA, and IgE and eosinophil cationic protein (ECP) levels were examined with RIA.

    RESULTS: After GC treatment, there was a statistically significant decrease of the T(H)2 cytokines IL-4, IL-6, and IL-10, as well as ECP and IgE. By contrast, there were no significant changes of the levels of IFN-gamma, IL-1beta, TNF-alpha, or neutrophils. In the GC-treated patients IL-1beta and TNF-alpha levels correlated with neutrophils and ECP, and IL-1beta correlated with eosinophils. Furthermore, ECP correlated with both eosinophils and neutrophils. Neither IL-1beta nor TNF-alpha correlated with IgE. Patients with high neutrophil counts after GC treatment were found to have significantly higher eosinophil counts and ECP than patients with low counts.

    CONCLUSIONS: The beneficial effects of topical treatment with GC in patients with allergic rhinitis could be attributed to downregulation of T(H)2 cytokines, with an ensuing decrease of eosinophils, ECP, and IgE. It is possible that neutrophils could counteract the beneficial effects of GCs by releasing the proinflammatory cytokines IL-1beta and TNF-alpha.

  • 7.
    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.
    The intrauterine and postnatal environments1999Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 104, nr 6, s. 1119-1127Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Pregnancy is associated with a strong skewing toward T(H)2 cytokine pattern, which enables the survival of the fetus, including fetal allergen-specific immune responses, The postnatal maturation of the immune system which is characterized by the development of a balanced T(H)1/T(H)2 immunity is genetically determined and modified by the environment. The process seems to proceed at a slower rate in atopic than in nonatopic infants. There is a close immunologic interaction between the mother and her offspring through the breast milk. Individual variations in the composition of human milk may el,plain the controversy with regard to the possible allergy-preventive effects of breast-feeding. Recurrent respiratory infections have been suggested to enhance immune deviation. The microbial flora are a more likely source, however, because they are a major driving force in the maturation of the immune system. Changes in its composition, as a consequence of an altered lifestyle and diet, may play a role in the higher prevalence of allergy. So far, primary prevention of allergy has failed. Future studies should therefore focus on factors enhancing immune deviation (ie, "success" factors) rather than on "risk" factors. The intestinal microflora is one of these factors that deserves closer analysis.

  • 8.
    Björkstén, Bengt
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Sepp, E
    Karolinska Inst, Ctr Allerg Res, S-17177 Stockholm, Sweden Linkoping Univ, Dept Paediat, S-58183 Linkoping, Sweden Univ Tartu, Dept Microbiol, EE-50090 Tartu, Estonia Univ Tartu, Dept Paediat, EE-50090 Tartu, Estonia.
    Julge, K
    Karolinska Inst, Ctr Allerg Res, S-17177 Stockholm, Sweden Linkoping Univ, Dept Paediat, S-58183 Linkoping, Sweden Univ Tartu, Dept Microbiol, EE-50090 Tartu, Estonia Univ Tartu, Dept Paediat, EE-50090 Tartu, Estonia.
    Voor, T
    Karolinska Inst, Ctr Allerg Res, S-17177 Stockholm, Sweden Linkoping Univ, Dept Paediat, S-58183 Linkoping, Sweden Univ Tartu, Dept Microbiol, EE-50090 Tartu, Estonia Univ Tartu, Dept Paediat, EE-50090 Tartu, Estonia.
    Mikelsaar, M
    Karolinska Inst, Ctr Allerg Res, S-17177 Stockholm, Sweden Linkoping Univ, Dept Paediat, S-58183 Linkoping, Sweden Univ Tartu, Dept Microbiol, EE-50090 Tartu, Estonia Univ Tartu, Dept Paediat, EE-50090 Tartu, Estonia.
    Allergy development and the intestinal microflora during the first year of life2001Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 108, nr 4, s. 516-520Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The intestinal microflora is a likely source for the induction of immune deviation in infancy. Objective: The purpose of this study was to prospectively relate the intestinal microflora to allergy development in 2 countries differing with respect to the prevalence of atopic diseases. Methods: Newborn infants were followed prospectively through the first 2 years of life in Estonia (n = 24) and Sweden (n = 20). By that age, 9 Estonian and 9 Swedish infants had developed atopic dermatitis and/or positive skin prick test results. Stool samples were obtained at 5 to 6 days and at 1, 3, 6, and 12 months, and 13 groups of aerobic and anaerobic microorganisms were cultivated through use of standard methods. Results: In comparison with healthy infants, babies who developed allergy were less often colonized with enterococci during the first month of life (72 % vs 96 %, P < .05) and with bifidobacteria during the first year of life (17 % to 39 % vs 42 % to 69 %, P < .05). Furthermore, allergic infants had higher counts of clostridia at 3 months (median value, 10.3 vs 7.2 log(10), P < .05). The prevalence of colonization with Staphylococcus aureus was also higher at 6 months (61 % vs 23 %, P < .05), whereas the counts of Bacteroides were lower at 12 months (9.9 vs 10.6 log(10), P < .05). Conclusion: Differences in the composition of the gut flora between infants who will and infants who will not develop allergy are demonstrable before the development of any clinical manifestations of atopy. Because the observations were made in 2 countries with different standards of living, we believe that our findings could indicate a role for the intestinal microflora in the development of and protection from allergy.

  • 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.
    The effects of breast milk on mitogen and allergen induced cytokine production from cord blood cells2001Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 107, nr 2, s. 261-Konferensbidrag (Övrigt vetenskapligt)
  • 10.
    Böttcher, Malin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Lindström, Annelie
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi.
    Jenmalm, Maria
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Bjorksten, B.
    Björkstén, B., Centre for Allergy Research, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.
    Vaarala, O.
    Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland.
    Reply [6]2006Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 117, nr 1, s. 220Övrigt (Övrigt vetenskapligt)
    Abstract [en]

    [No abstract available]

  • 11.
    Casas, Rosaura
    et al.
    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.
    Detection of IgA antibodies to cat, Der p 1 and Bet v 1 inhalant allergens in human milk2001Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 107, nr 2, s. 97-Konferensbidrag (Övrigt vetenskapligt)
  • 12.
    Casas, Rosaura
    et al.
    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.
    Jenmalm, Maria
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Cat allergen induced cytokine secretion and Fel d 1-IgG immune complexes in cord blood2002Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 109, nr 1, s. 529-Konferensbidrag (Övrigt vetenskapligt)
  • 13.
    Casas, Rosaura
    et al.
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Böttcher, Malin
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Duchén, Karel
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Björkstén, Bengt
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Detection of IgA antibodies to cat, β-lactoglobulin, and ovalbumin allergens in human milk2000Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 105, nr 6 part 1, s. 1236-1240Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The relationship between the development of allergy during infancy and breast-feeding remains controversial. This controversy may be due to individual variations in the composition of human milk. Antibodies to food antigens to which the mother is commonly exposed are present in the milk, but their relationship to allergy is still unknown. IgA antibodies to inhalant allergens have not been previously detected.

    Objective: Our purpose was to analyze secretory IgA antibody levels to cat, β-lactoglobulin, and ovalbumin allergens in colostrum and mature milk in relation to maternal allergy.

    Methods: Colostrum and samples of mature milk were obtained after 1 and 3 months of lactation from 53 nursing mothers (17 allergic and 36 nonallergic mothers) and were analyzed for total secretory IgA levels by ELISA and secretory IgA antibodies to cat, β-lactoglobulin, and ovalbumin by an enzyme-amplified ELISA. The specificity of the assays was confirmed by inhibition experiments.

    Results: Secretory IgA to cat, β-lactoglobulin, and ovalbumin allergens were detected in colostrum as well as mature milk. The levels of secretory IgA to ovalbumin were lower in colostrum from allergic mothers with P = .016, whereas the levels to β-lactoglobulin and cat were similar in the 2 groups. IgA antibodies to ovalbumin were detected in 94% of the colostrum samples from allergic and in all samples from nonallergic mothers, in 82% and 96%, respectively at 1 month, and 53% and 65% at 3 months. Fewer samples had detectable secretory IgA antibodies to β-lactoglobulin than to ovalbumin and cat, and only 33% and 10% of the samples from the allergic and nonallergic mothers, respectively, remained positive at 3 months. All the allergic mothers had detectable IgA to cat in colostrum, whereas 83% and 73% of the samples were positive at 1 and 3 months. The corresponding numbers were 93%, 81%, and 81% in the nonallergic mothers (not significant).

    Conclusion: Even a low level of exposure of the mucosa (eg, by inhalant allergens) can induce antibody secretion into the milk, both in allergic and nonallergic mothers. (J Allergy Clin Immunol 2000;105:1236-40.)

  • 14.
    Christmann, Benjamin S.
    et al.
    University of Alabama Birmingham, AL 35294 USA.
    Abrahamsson, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Region Östergötland, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping. Linköpings universitet, Medicinska fakulteten.
    Bernstein, Charles N.
    University of Manitoba, Canada.
    Wayne Duck, L.
    University of Alabama Birmingham, AL 35294 USA.
    Mannon, Peter J.
    University of Alabama Birmingham, AL 35294 USA.
    Berg, Göran
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
    Bjorksten, Bengt
    Karolinska Institute, Sweden; University of Örebro, Sweden.
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Elson, Charles O.
    University of Alabama Birmingham, AL 35294 USA.
    Human seroreactivity to gut microbiota antigens2015Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 136, nr 5, s. 1378-1386Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Although immune responses directed against antigens from the intestinal microbiota are observed in certain diseases, the normal human adaptive immune response to intestinal microbiota is poorly defined. Objective: Our goal was to assess the adaptive immune response to the intestinal microbiota present in 143 healthy adults and compare this response with the response observed in 52 children and their mothers at risk of having allergic disease. Methods: Human serum was collected from adults and children followed from birth to 7 years of age, and the serum IgG response to a panel of intestinal microbiota antigens was assessed by using a novel protein microarray. Results: Nearly every subject tested, regardless of health status, had serum IgG that recognized a common set of antigens. Seroreactivity to the panel of antigens was significantly lower in atopic adults. Healthy infants expressed the highest level of IgG seroreactivity to intestinal microbiota antigens. This adaptive response developed between 6 and 12 months of age and peaked around 2 years of age. Low IgG responses to certain clusters of microbiota antigens during infancy were associated with allergy development during childhood. Conclusions: There is an observed perturbation of the adaptive response to antigens from the microbiota in allergic subjects. These perturbations are observable even in childhood, suggesting that optimal stimulation of the adaptive immune system by the microbiota might be needed to prevent certain immune-mediated diseases.

  • 15.
    Dzidic, Majda
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. FISABIO Fdn, Spain; Spanish National Research Council, 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, Barn- och ungdomskliniken i Linköping.
    Artacho, Alejandro
    FISABIO Fdn, Spain.
    Björksten, Bengt
    Karolinska Institute, Sweden.
    Collado, Maria Carmen
    Spanish National Research Council, Spain.
    Mira, Alex
    FISABIO Fdn, Spain.
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Aberrant IgA responses to the gut microbiota during infancy precede asthma and allergy development2017Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 139, nr 3, s. 1017-+Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Although a reduced gut microbiota diversity and low mucosal total IgA levels in infancy have been associated with allergy development, IgA responses to the gut microbiota have not yet been studied. Objective: We sought to determine the proportions of IgA coating together with the characterization of the dominant bacteria, bound to IgA or not, in infant stool samples in relation to allergy development. Methods: A combination of flow cytometric cell sorting and deep sequencing of the 16S rDNA gene was used to characterize the bacterial recognition patterns by IgA in stool samples collected at 1 and 12 months of age from children staying healthy or having allergic symptoms up to 7 years of age. Results: The children with allergic manifestations, particularly asthma, during childhood had a lower proportion of IgA bound to fecal bacteria at 12months of age compared with healthy children. These alterations cannot be attributed to differences in IgA levels or bacterial load between the 2 groups. Moreover, the bacterial targets of early IgA responses (including coating of the Bacteroides genus), as well as IgA recognition patterns, differed between healthy children and children with allergic manifestations. Altered IgA recognition patterns in children with allergy were observed already at 1 month of age, when the IgA antibodies are predominantly maternally derived in breast-fed children. Conclusion: An aberrant IgAresponsiveness to the gutmicrobiota during infancy precedes asthma and allergy development, possibly indicating an impaired mucosal barrier function in allergic children.

  • 16. Estelle, F
    et al.
    Simons, R
    Kjellman, Max
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Prospective, long-term safety evaluation of the H1-receptor antagonist cetirizine in very young children with atopic dermatitis.1999Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 104, s. 433-440Artikel i tidskrift (Refereegranskat)
  • 17.
    Fagerås Böttcher, Malin
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Hmani-Aifa, Mounira
    Linköpings universitet, Institutionen för biomedicin och kirurgi. Linköpings universitet, Hälsouniversitetet.
    Lindström Lundberg, Anna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Jenmalm, Maria Christina
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Mai, Xiao-Mei
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Nilsson, Lennart
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Aniansson Zdolsek, Helena
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Björkstén, Bengt
    Centre for Allergy Research and Institute of Environmental Medicine, Karolinska Institute, Stockholm;.
    Söderkvist, Peter
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Vaarala, Outi
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    A TLR4 polymorphism is associated with asthma and reduced lipopolysaccharide-induced interleukin-12(p70) responses in Swedish children2004Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 114, nr 3, s. 561-567Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    Bacterial signals play an important role in the maturation of the immune system. Polymorphisms in genes coding for receptors to bacterial components can alter the immune responsiveness of the host to microbial agents and may indicate the development of aberrant immune responses that are associated with immune-mediated diseases such as atopic diseases.

    Objective

    The study's objective was to investigate the relationship between TLR4 and CD14 gene polymorphisms, the LPS responsiveness of PBMCs, and the presence of asthma and allergic rhinoconjunctivitis in children.

    Methods

    The TLR4 (Asp299Gly) and CD14/−159 polymorphisms were determined in 115 Swedish children aged 8 and 14 years. LPS-induced IL-12(p70), IL-10, and IFN-γ responses of PBMCs from 69 of the children were analyzed by means of ELISA. The levels of soluble CD14 in serum samples were analyzed by means of ELISA, and the total IgE levels were analyzed by means of UniCAP Total IgE (Pharmacia Diagnostics, Uppsala, Sweden).

    Results

    Decreased LPS-induced IL-12(p70) and IL-10 responses were associated with the TLR4 (Asp299Gly) polymorphism and independently with asthma, especially atopic asthma. The TLR4 (Asp299Gly) polymorphism was associated with a 4-fold higher prevalence of asthma in school-aged children (adjusted odds ratio 4.5, 95% CI 1.1-17.4) but not to allergic rhinoconjunctivitis.

    Conclusion

    A TLR4 polymorphism modifies innate immune responses in children and may be an important determinant for the development of asthma. This may influence the outcome of intervention studies that use microbial stimuli as immune modulators.

  • 18.
    Forsberg, Anna
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för inflammationsmedicin. Linköpings universitet, Hälsouniversitetet.
    Bengtsson, Mathias
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för inflammationsmedicin. Linköpings universitet, Hälsouniversitetet.
    Eringfält, Anna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för inflammationsmedicin. Linköpings universitet, Hälsouniversitetet.
    Ernerudh, Jan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för inflammationsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Diagnostikcentrum, Klinisk immunologi och transfusionsmedicin.
    Mjösberg, Jenny
    Department of Medicine, Center for Infectious Medicine, Karolinska University Hospital Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för inflammationsmedicin. Linköpings universitet, Hälsouniversitetet.
    Letter: GATA binding protein 3(+) group 2 innate lymphoid cells are present in cord blood and in higher proportions in male than in female neonates.2014Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 134, nr 1, s. 228-230Artikel i tidskrift (Refereegranskat)
  • 19.
    Hellberg, Sandra
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Bhai Mehta, Ratnesh
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Forsberg, Anna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Berg, Göran
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
    Brynhildsen, Jan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
    Winqvist, Ola
    Karolinska Inst, Sweden.
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Ernerudh, Jan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk immunologi och transfusionsmedicin.
    Maintained thymic output of conventional and regulatory T cells during human pregnancy2019Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 143, nr 2, s. 771-775.e7Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    n/a

  • 20.
    Jenmalm, Maria
    et al.
    Linköpings universitet, Institutionen för hälsa och miljö. Linköpings universitet, Hälsouniversitetet.
    Björkstén, Bengt
    Linköpings universitet, Institutionen för hälsa och miljö. Linköpings universitet, Hälsouniversitetet.
    Exposure to cow's milk during the first 3 months of life is associated with increased levels of IgG subclass antibodies to beta-lactoglobulin to 8 years1998Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 102, s. 671-678Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND:

    Exposure to allergens early in life influences the development of allergen-specific immune responses. In animal models, the development of tolerance to proteins delivered to the gastrointestinal and the respiratory mucosa is influenced by age and genetic background. Late introduction of cow's milk in infants is associated with slower increase and lower peak IgG antibody responses to milk during early childhood, but the long-term effects have not been investigated, nor is the relation to atopic disease later in life clear.

    OBJECTIVE:

    The purpose of this study was to investigate the development of IgG subclass antibodies to beta-lactoglobulin in relation to early exposure to cow's milk, atopic heredity, and the development of atopic disease.

    METHODS:

    IgG subclass antibodies to beta-lactoglobulin were analyzed by ELISA at birth, at 6 and 18 months, and at 8 years in 96 children followed prospectively.

    RESULTS:

    The levels of IgG subclass antibodies to beta-lactoglobulin peaked in early childhood and then declined up to 8 years of age. Exposure to cow's milk during the first 3 months of life was associated with high IgG subclass antibody levels to beta-lactoglobulin up to 8 years, particularly in children with maternal atopy. Children with atopic symptoms and sensitivity to allergens often had high levels of IgG4 antibodies to beta-lactoglobulin at 8 years of age, even if they were not exposed to cow's milk during the first 3 months of life. Furthermore, atopic dermatitis was associated with high levels of IgG subclass antibodies to beta-lactoglobulin in early childhood.

    CONCLUSIONS:

    IgG subclass antibody levels to milk peak during early infancy, with particularly high levels in children with atopic dermatitis, and decline thereafter. Exposure to cow's milk during early infancy has long-lasting effects on the humoral antigen-specific responses, indicating less effective tolerance-inducing mechanisms in the intestinal mucosa during the first months of life.

  • 21.
    Jenmalm, Maria
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik.
    Macaubas, C
    Fac Hlth Sci, Div Paediat, Linkoping, Sweden TVW Telethon Inst Child Hlth Res, Perth, WA, Australia.
    Holt, P
    Holt, B
    Smallacombe, T
    Fac Hlth Sci, Div Paediat, Linkoping, Sweden TVW Telethon Inst Child Hlth Res, Perth, WA, Australia.
    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.
    Allergen induced cytokine responses at birth in relation to development of atopic disease and sensitisation2000Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 105, nr 1, s. 329-Konferensbidrag (Övrigt vetenskapligt)
  • 22.
    Konya, Viktoria
    et al.
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Czarnewski, Paulo
    Sci Life Lab, Sweden.
    Forkel, Marianne
    Karolinska Inst, Sweden.
    Rao, Anna
    Karolinska Inst, Sweden.
    Kokkinou, Efthymia
    Karolinska Inst, Sweden.
    Villablanca, Eduardo J.
    Sci Life Lab, Sweden.
    Almer, Sven
    Karolinska Univ Hosp, Sweden.
    Lindforss, Ulrik
    Karolinska Univ Hosp, Sweden.
    Friberg, Danielle
    Karolinska Univ Hosp, Sweden.
    Hoeoeg, Charlotte
    Karolinska Univ Hosp, Sweden.
    Bergman, Peter
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Mjösberg, Jenny
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden.
    Vitamin D downregulates the IL-23 receptor pathway in human mucosal group 3 innate lymphoid cells2018Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 141, nr 1, s. 279-292Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Vitamin D deficiency is a risk factor for inflammatory bowel disease (IBD). The IL-23-driven tissue-resident group 3 innate lymphoid cells (ILC3s) play essential roles in intestinal immunity, and targeting IL-23/12 is a promising approach in IBD therapy. Objective: We set out to define the role of 1 alpha,25-dihydroxy vitamin D3 (1,25D) in regulating functional responses of human mucosal ILC3s to IL-23 plus Il-1 beta stimulation. Methods: Transcriptomes of sorted tonsillar ILC3s were assessed by using microarray analysis. ILC3 cytokine production, proliferation, and differentiation were determined by means of flow cytometry, ELISA, and multiplex immunoassay. Intestinal cell suspensions and ILC3s sorted from gut biopsy specimens of patients with IBD were also analyzed along with plasma 25-hydroxy vitamin D3 (25D) detection. Results: ILC3s stimulated with IL-23 plus IL-1 beta upregulated the vitamin D receptor and responded to 1,25D with downregulation of the IL-23 receptor pathway. Consequently, 1,25D suppressed IL-22, IL-17F, and GM-CSF production from tonsillar and gut ILC3s. In parallel, 1,25D upregulated genes linked to the IL-1 beta signaling pathway, as well as the IL-1 beta-inducible cytokines IL-6, IL-8, and macrophage inflammatory protein IL/1 beta. The 1,25D-triggered skewing in ILC3 function was not accompanied or caused by changes in viability, proliferation, or phenotype. Finally, we confirmed low 25D plasma levels in patients with IBD with active inflammation. Conclusion: In light of the beneficial targeting of IL-23/12 in patients with IBD, 1,25D appears as an interesting therapeutic agent that inhibits the IL-23 receptor pathway, providing a novel mechanism for how ILC3s could be manipulated to regulate intestinal inflammation.

  • 23. Liu, X
    et al.
    Nickel, R
    Beyer, K
    Wahn, U
    Ehrilick, E
    Freidhoff, R
    Björkstén, B
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Beaty, TH
    Huang, S-K
    An IL13 coding region variant is associated with a high total serum IgE level and atopic dermatitis in the German Multicenter Atopy Study (MAS-90)2000Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 106, nr 1 I, s. 167-170Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Allergic diseases are one of the major causes of morbidity in the developed countries today, and the prevalence of these diseases is increasing steadily. Study of total serum IgE level is important in understanding the genetics of allergic diseases because IgE levels are considered to be a crucial pathogenic component. IL-13 plays an important role in the induction of IgE synthesis and in the pathogenesis of allergic diseases. Objective: We sought to examine potential variation at the IL13 gene and estimate its effect on elevated IgE level and atopic dermatitis (AD). Methods: We conducted mutational analyses of the IL13 gene by using single-stranded conformation polymorphism and DNA sequencing. Case control studies for high-IgE phenotype and AD were performed by using subjects from the German MAS-90 cohort. Results: A novel IL13 coding region variant at 4257 bp (G to A, fourth exon) was identified. Case control studies of a German sample from the MAS-90 cohort showed significant associations between the presence of the A allele and two atopic phenotypes: high IgE (odds ratio, 2.38, 95% confidence interval, 1.35-4.21, P = .0026) and AD (odds ratio, 1.77, 95% confidence interval, 1.06-2.96, P = .03). Conclusion: This IL13 coding region variant may be involved in the pathogenesis of AD and high total serum IgE level in a study population of white subjects.

  • 24.
    Maric, Jovana
    et al.
    Med Univ Graz, Austria; Karolinska Inst, Sweden.
    Ravindran, Avinash
    Karolinska Inst, Sweden.
    Mazzurana, Luca
    Karolinska Inst, Sweden.
    Bjorklund, Asa K.
    Uppsala Univ, Sweden.
    Van Acker, Aline
    Karolinska Inst, Sweden.
    Rao, Anna
    Karolinska Inst, Sweden.
    Friberg, Danielle
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Dahlen, Sven-Erik
    Karolinska Inst, Sweden.
    Heinemann, Akos
    Med Univ Graz, Austria.
    Konya, Viktoria
    Med Univ Graz, Austria; Karolinska Inst, Sweden.
    Mjösberg, Jenny
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden.
    Prostaglandin E-2 suppresses human group 2 innate lymphoid cell function2018Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 141, nr 5, s. 1761-+Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Group 2 innate lymphoid cells (ILC2s) are involved in the initial phase of type 2 inflammation and can amplify allergic immune responses by orchestrating other type 2 immune cells. Prostaglandin (PG) E-2 is a bioactive lipid that plays protective roles in the lung, particularly during allergic inflammation. Objective: We set out to investigate how PGE(2) regulates human ILC2 function. Methods: The effects of PGE(2) on human ILC2 proliferation and intracellular cytokine and transcription factor expression were assessed by means of flow cytometry. Cytokine production was measured by using ELISA, and real-time quantitative PCR was performed to detect PGE(2) receptor expression. Results: PGE(2) inhibited GATA-3 expression, as well as production of the type 2 cytokines IL-5 and IL-13, from human tonsillar and blood ILC2s in response to stimulation with a combination of IL-25, IL-33, thymic stromal lymphopoietin, and IL-2. Furthermore, PGE(2) downregulated the expression of IL-2 receptor alpha (CD25). In line with this observation, PGE(2) decreased ILC2 proliferation. These effects were mediated by the combined action of E-type prostanoid receptor (EP) 2 and EP4 receptors, which were specifically expressed on ILC2s. Conclusion: Our findings reveal that PGE(2) limits ILC2 activation and propose that selective EP2 and EP4 receptor agonists might serve as a promising therapeutic approach in treating allergic diseases by suppressing ILC2 function.

  • 25.
    Maric, Jovana
    et al.
    Med Univ Graz, Austria; BioTechMed, Austria; Karolinska Inst, Sweden.
    Ravindran, Avinash
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Mazzurana, Luca
    Karolinska Inst, Sweden.
    Van Acker, Aline
    Karolinska Inst, Sweden.
    Rao, Anna
    Karolinska Inst, Sweden.
    Kokkinou, Efthymia
    Karolinska Inst, Sweden.
    Ekoff, Maria
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Thomas, Dominique
    Goethe Univ Frankfurt, Germany.
    Fauland, Alexander
    Karolinska Inst, Sweden.
    Nilsson, Gunnar
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden; Uppsala Univ, Sweden.
    Wheelock, Craig E.
    Karolinska Inst, Sweden.
    Dahlen, Sven-Erik
    Karolinska Inst, Sweden.
    Ferreiros, Nerea
    Goethe Univ Frankfurt, Germany.
    Geisslinger, Gerd
    Goethe Univ Frankfurt, Germany; Fraunhofer Inst Mol Biol and Appl Ecol IME, Germany.
    Friberg, Danielle
    Karolinska Inst, Sweden; Uppsala Univ, Sweden.
    Heinemann, Akos
    Med Univ Graz, Austria; BioTechMed, Austria.
    Konya, Viktoria
    Med Univ Graz, Austria; BioTechMed, Austria; Karolinska Inst, Sweden.
    Mjösberg, Jenny
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden.
    Cytokine-induced endogenous production of prostaglandin D-2 is essential for human group 2 innate lymphoid cell activation2019Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 143, nr 6, s. 2202-+Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: We set out to examine PG production in human ILC2s and the implications of such endogenous production on ILC2 function. Methods: The effects of the COX-1/2 inhibitor flurbiprofen, the hematopoietic prostaglandin D2 synthase (HPGDS) inhibitor KMN698, and the CRTH2 antagonist CAY10471 on human ILC2s were determined by assessing receptor and transcription factor expression, cytokine production, and gene expression with flow cytometry, ELISA, and quantitative RT-PCR, respectively. Concentrations of lipid mediators were measured by using liquid chromatography-tandem mass spectrometry and ELISA. Results: We show that ILC2s constitutively express HPGDS and upregulate COX-2 upon IL-2, IL-25, and IL-33 plus thymic stromal lymphopoietin stimulation. Consequently, PGD2 and its metabolites can be detected in ILC2 supernatants. We reveal that endogenously produced PGD2 is essential in cytokine-induced ILC2 activation because blocking of the COX-1/2 or HPGDS enzymes or the CRTH2 receptor abolishes ILC2 responses. Conclusion: PGD2 produced by ILC2s is, in a paracrine/autocrine manner, essential in cytokine-induced ILC2 activation. Hence we provide the detailed mechanism behind how CRTH2 antagonists represent promising therapeutic tools for allergic diseases by controlling ILC2 function.

  • 26.
    Möller, Christian
    et al.
    Department of Paediatrics, Umeå University.
    Dreborg, Sten
    Department of Paediatrics, University Hospital of Oslo.
    Ferdousi, Hosne Ara
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Halken, Susanne
    Department of Paediatrics, Hospital of Sønderborg.
    Høst, Arne
    Department of Paediatrics, University Hospital of Odense.
    Jacobsen, Lars
    ALK-Abelló, Hørsholm.
    Koivikko, Antti
    Turku Allergy Centre.
    Koller, Dieter Y.
    University Children’s Hospital, Vienna.
    Niggemann, Bodo
    University Children’s Hospital, Vienna.
    Norberg, Lene A.
    Department of Paediatrics, University Hospital of Odense.
    Urbanek, Radvan
    University Children’s Hospital, Vienna.
    Valovirta, Erkka
    Turku Allergy Centre.
    Wahn, Ulrich
    University Children’s Hospital of Charité, Berlin.
    Pollen immunotherapy reduces the development of asthma in children with seasonal rhinoconjunctivitis (the PAT-study)2002Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 109, nr 2, s. 251-256Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Children with allergic rhinitis are likely to develop asthma.

    Objective: The purpose of this investigation was to determine whether specific immunotherapy can prevent the development of asthma and reduce bronchial hyperresponsiveness in children with seasonal allergic rhinoconjunctivitis.

    Methods: From 6 pediatric allergy centers, 205 children aged 6 to 14 years (mean age, 10.7 years) with grass and/or birch pollen allergy but without any other clinically important allergy were randomized either to receive specific immunotherapy for 3 years or to an open control group. All subjects had moderate to severe hay fever symptoms, but at inclusion none reported asthma with need of daily treatment. Symptomatic treatment was limited to loratadine, levocabastine, sodium cromoglycate, and nasal budesonide. Asthma was evaluated clinically and by peak flow. Methacholine bronchial provocation tests were carried out during the season(s) and during the winter.

    Results: Before the start of immunotherapy, 20% of the children had mild asthma symptoms during the pollen season(s). Among those without asthma, the actively treated children had significantly fewer asthma symptoms after 3 years as evaluated by clinical diagnosis (odds ratio, 2.52; P < .05). Methacholine bronchial provocation test results improved significant in the active group (P < .05).

    Conclusion: Immunotherapy can reduce the development of asthma in children with seasonal rhinoconjunctivitis.

  • 27. Paronen, J
    et al.
    Björkstén, B
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Hattevig, G
    Åkerblom, H
    Vaarala, O
    Effect of maternal diet during lactation on development of bovine insulin-binding antibodies in children at risk for allergy2000Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 106, nr 2, s. 302-306Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The role of exposure to dietary antigens through maternal milk is intriguing, because it may result either in immunization or in tolerance. Exposure to cow's milk proteins results in antibody formation against bovine insulin in infants at risk for type 1 diabetes. Objective: To study the appearance of IgG antibodies to bovine and human insulin in infants with an atopic family history whose mothers followed a cow's milk-free diet during the first 3 months of lactation. Methods: In a prospective cohort study on prevention of food allergies, 123 infants were exclusively breast-fed or received supplementafion with a hydrolyzed casein-based formula (Nutramigen) until the age of 6 months. The mothers either avoided cow's milk during the first 3 months of lactation (diet group) or had an unrestricted diet (nondiet group). The levels of IgG antibodies to bovine and human insulin were determined by enzyme immunoassay at 3, 6, 12, and 18 months and at 4 years. In addition, cord blood was obtained at birth and a maternal sample at delivery. Results: At 3 months, IgG antibodies to bovine insulin were low in both dietary groups (median levels 0.150 and 0.114 optical density units in the diet and nondiet groups). After exposure to dietary insulin, IgG antibodies to bovine insulin increased in both groups, reaching a peak at 12 months in the nondiet group and at 18 months in the diet group. At 18 months, IgG antibodies to bovine insulin were lower in infants in the nondiet group than in infants in the diet group (0.287 vs 0.500, P < .0001). At 4 years, the antibodies no longer differed between the groups. Conclusion: The exposure to cow's milk proteins through breast milk during the first 3 months of life resulted in decreased levels of antibodies to dietary bovine insulin at 18 months of age, suggesting a role for breast milk antigens in early tolerance induction.

  • 28.
    Pohjavuori, Emma
    et al.
    Hospital for Children and Adolescents Helsingfors, Finland.
    Viljanen, Mirva
    Skin and Allergy Hospital Helsingfors, Finland.
    Korpela, Riita
    Inst of Biomedicine, Pharmacology Helsingfors Universitet, Finland.
    Kuitunen, Mikael
    Skin and Allergy Hospital Helsingfors, Finland.
    Tiittanen, Minna
    Dept of Molecular Medicine Helsingfors, Finland.
    Vaarala, Outi
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Savilahti, Erkki
    Hospital for Children and Adolescents Helsingfors, Finland.
    Lactobacillus GG effect in increasing IFN-gamma production in infants with cow's milk allergy.2004Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 114, s. 131-136Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Probiotic bacteria are potentially beneficial to maturation of the infant's immune system. Objective: To examine the role of probiotic bacteria in treatment of cow's milk allergy (CMA) and IgE-associated dermatitis, we investigated the immunologic effects of Lactobacillus rhamnosus GG (LGG) and a mixture of 4 bacterial species (MIX). Methods: In a randomized, double-blind study design, concomitantly with elimination diet and skin treatment, LGG, MIX, or placebo was given for 4 weeks to infants with suspected CMA. After anti-CD3 (OKT3) and anti-CD28 stimulation of PBMCs, IFN-gamma, IL-4, IL-5, and IL-12 levels were measured in culture supernatants by ELISA. Intracellular IFN-gamma, IL-4, and IL-5 production on CD4 lymphocytes was analyzed with fluorescence-activated cell sorting. Results: Secretion of IFN-gamma by PBMCs before the treatment was significantly lower in infants with CMA (P = .016) and in infants with IgE-associated CMA (P = .003) than in non-CMA infants. Among the infants who received LGG, the level of secreted IFN-gamma increased in those with CMA (P = .006) and in those with IgE-associated dermatitis (P = .017) when compared with the placebo group. Secretion of IL-4 increased significantly in infants with CMA in the MIX (P = .034) but not in the LGG group. Conclusion: Deficiency in IFN-gamma response appears to be related to CMA. LGG raises IFN-gamma production of PBMC in infants with CMA and in infants with IgE-associated dermatitis and may thus provide beneficial T(H)1 immunomodulatory signals. MIX, although containing LGG, appears to modulate the immune responses differently.

  • 29.
    Ringsberg, K
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för hälsa och samhälle, Socialmedicin och folkhälsovetenskap.
    Åkerlind, I
    FoU enheten Norrköping.
    Presence of hyperventilation in patients with asthma-like symptoms but negative asthma test responses: Provocation with voluntary hyperventilation and mental stress. 1999Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 103, s. 601-608Artikel i tidskrift (Refereegranskat)
  • 30.
    Sonnenschein-van der Voort, Agnes M. M
    et al.
    Erasmus MC, Netherlands Erasmus MC, Netherlands Erasmus MC, Netherlands .
    Arends, Lidia R.
    Erasmus MC, Netherlands Erasmus University, Netherlands Erasmus University, Netherlands .
    de Jongste, Johan C.
    Erasmus Medical Center, Rotterdam, The Netherlands.
    Annesi-Maesano, Isabella
    Erasmus MC, Netherlands INSERM, France University of Paris 06, France .
    Arshad, S. Hasan
    St Marys Hospital, England .
    Barros, Henrique
    University of Porto, Portugal .
    Basterrechea, Mikel
    Public Health Div Gipuzkoa, Spain Spanish Consortium Research Epidemiol and Public Health CIBE, Spain .
    Bisgaard, Hans
    University of Copenhagen, Denmark Copenhagen University Hospital, Denmark .
    Chatzi, Leda
    University of Crete, Greece .
    Corpeleijn, Eva
    University of Groningen, Netherlands .
    Correia, Sofia
    University of Porto, Portugal .
    Craig, Leone C.
    University of Aberdeen, Scotland .
    Devereux, Graham
    University of Aberdeen, Scotland .
    Dogaru, Cristian
    University of Bern, Switzerland .
    Dostal, Miroslav
    Academic Science Czech Republic, Czech Republic .
    Duchén, Karel
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
    Eggesbo, Merete
    Norwegian Institute Public Heatlh, Norway .
    Kors van der Ent, C.
    University of Medical Centre Utrecht, Netherlands .
    Fantini, Maria P.
    University of Bologna, Bologna, Italy.
    Forastiere, Francesco
    Lazio Regional Health Serv, Italy .
    Frey, Urs
    University of Basel, Switzerland .
    Gehring, Ulrike
    University of Utrecht, Netherlands .
    Gori, Davide
    University of Bologna, Bologna, Italy.
    van der Gugten, AnneC.
    University of Medical Centre Utrecht, Netherlands .
    Hanke, Wojciech
    Nofer Institute Occupat Med, Poland .
    Henderson, A. John
    University of Bristol, England .
    Heude, Barbara
    INSERM, France University of Paris 11, France .
    Iniguez, Carmen
    Spanish Consortium Research Epidemiol and Public Health CIBE, Spain University of Valencia, Spain University of Valencia, Spain .
    Inskip, Hazel M.
    University of Southampton, England .
    Keil, Thomas
    Charite, Germany University of Wurzburg, Germany .
    Kelleher, CecilyC.
    University of Coll Dublin, Ireland .
    Kogevinas, Manolis
    National School Public Heatlh, Greece .
    Kreiner-Moller, Eskil
    University of Copenhagen, Denmark Copenhagen University Hospital, Denmark .
    Kuehni, Claudia E.
    University of Bern, Switzerland .
    Kuepers, LeanneK.
    University of Groningen, Netherlands .
    Lancz, Kinga
    Slovak Medical University, Slovakia .
    Larsen, PernilleS.
    University of Copenhagen, Denmark .
    Lau, Susanne
    Charite, Germany .
    Ludvigsson, Johnny
    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.
    Mommers, Monique
    Maastricht University, Netherlands .
    Nybo Andersen, Anne-Marie
    University of Copenhagen, Denmark .
    Palkovicova, Lubica
    Slovak Medical University, Slovakia .
    Pike, Katharine C.
    University of Southampton, England .
    Pizzi, Costanza
    University of Turin, Italy .
    Polanska, Kinga
    Nofer Institute Occupat Med, Poland .
    Porta, Daniela
    Lazio Regional Health Serv, Italy .
    Richiardi, Lorenzo
    University of Turin, Italy .
    Roberts, Graham
    St Marys Hospital, England .
    Schmidt, Anne
    University of Bern, Switzerland .
    Sram, RadimJ.
    Academic Science Czech Republic, Czech Republic .
    Sunyer, Jordi
    St Marys Hospital, England Spanish Consortium Research Epidemiol and Public Health CIBE, Spain Centre Research Environm Epidemiol CREAL, Spain Pompeu Fabra University, Spain Hospital del Mar, Spain .
    Thijs, Carel
    Maastricht University, Netherlands .
    Torrent, Maties
    University of Bologna, Italy .
    Viljoen, Karien
    University of Coll Dublin, Ireland .
    Wijga, Alet H.
    National Institute Public Health and Environm RIVM, Netherlands .
    Vrijheid, Martine
    St Marys Hospital, England Spanish Consortium Research Epidemiol and Public Health CIBE, Spain Centre Research Environm Epidemiol CREAL, Spain Pompeu Fabra University, Spain .
    Jaddoe, VincentW . V.
    Erasmus MC, Netherlands Erasmus MC, Netherlands Erasmus MC, Netherlands .
    Duijts, Liesbeth
    Erasmus MC, Netherlands Erasmus MC, Netherlands Erasmus MC, Netherlands .
    Preterm birth, infant weight gain, and childhood asthma risk: A meta-analysis of 147,000 European children2014Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 133, nr 5, s. 1317-1329Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Preterm birth, low birth weight, and infant catch-up growth seem associated with an increased risk of respiratory diseases in later life, but individual studies showed conflicting results. Objectives: We performed an individual participant data meta-analysis for 147,252 children of 31 birth cohort studies to determine the associations of birth and infant growth characteristics with the risks of preschool wheezing (1-4 years) and school-age asthma (5-10 years). Methods: First, we performed an adjusted 1-stage random-effect meta-analysis to assess the combined associations of gestational age, birth weight, and infant weight gain with childhood asthma. Second, we performed an adjusted 2-stage random-effect meta-analysis to assess the associations of preterm birth (gestational age less than 37 weeks) and low birth weight (less than 2500 g) with childhood asthma outcomes. Results: Younger gestational age at birth and higher infant weight gain were independently associated with higher risks of preschool wheezing and school-age asthma (P less than. 05). The inverse associations of birth weight with childhood asthma were explained by gestational age at birth. Compared with term-born children with normal infant weight gain, we observed the highest risks of school-age asthma in children born preterm with high infant weight gain (odds ratio [OR], 4.47; 95% CI, 2.58-7.76). Preterm birth was positively associated with an increased risk of preschool wheezing (pooled odds ratio [pOR], 1.34; 95% CI, 1.25-1.43) and school-age asthma (pOR, 1.40; 95% CI, 1.18-1.67) independent of birth weight. Weaker effect estimates were observed for the associations of low birth weight adjusted for gestational age at birth with preschool wheezing (pOR, 1.10; 95% CI, 1.00-1.21) and school-age asthma (pOR, 1.13; 95% CI, 1.01-1.27). Conclusion: Younger gestational age at birth and higher infant weight gain were associated with childhood asthma outcomes. The associations of lower birth weight with childhood asthma were largely explained by gestational age at birth.

  • 31. van Hage-Hamsten, M
    et al.
    Kronqvist, M
    Zetterström, Olle
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för hälsa och miljö. Östergötlands Läns Landsting, Medicincentrum, Allergicentrum US.
    Johansson, E
    Niederberger, V
    Vertala, S
    Gronlund, H
    Gronneberg, R
    Valenta, R
    Skin test evaluation of genetically engineered hypoallergenic derivatives pollen allergen, Bet v 1: trimer in a Swedish population before the birch pollen season.1999Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 104, s. 969-977Artikel i tidskrift (Refereegranskat)
  • 32.
    Viljanen, Mirva
    et al.
    Finland .
    Pohjavuori, Emma
    Finland .
    Haahtela, Tari
    Finland .
    Korpela, Riitta
    Finland .
    Kuitunen, Mikael
    Finland .
    Sarnesto, Annikki
    Finland .
    Vaarala, Outi
    National Public Health Institute, Helsinki.
    Savilahti, Erkki
    Finland .
    Induction of inflammation as a possible mechanism of probiotic effect in atopic ezema-dermatitis syndrome2005Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 115, nr 6, s. 1254-1259Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    The immunomodulating mechanisms of Lactobacillus GG (LGG) and other probiotics are poorly understood.

    Objective

    We studied in vivo the immunologic effects of probiotics in infants with atopic eczema–dermatitis syndrome (AEDS) and cow's milk allergy (CMA).

    Methods

    Two hundred thirty infants with AEDS and suspected CMA received, concomitant with elimination diet, either LGG, a mixture of 4 probiotic strains (MIX), or placebo for 4 weeks. All available paired pretreatment and posttreatment plasma samples (n = 132) were analyzed for concentrations of IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-γ, soluble intercellular adhesion molecule 1, soluble E-selectin, TGF-β1, TGF-β2, and C-reactive protein.

    Results

    In infants with IgE-associated AEDS, treatment with LGG induced higher C-reactive protein levels than in the placebo group (geometric mean, 0.83 μg/mL [95% CI, 0.56-0.81] vs 0.42 μg/mL [95% CI, 0.27-0.65]; P = .021). Concomitantly, IL-6 levels increased after treatment with LGG (P = .023) but not with MIX or placebo. Soluble E-selectin levels were higher after probiotic than after placebo treatment in infants with IgE-mediated CMA (LGG geometric mean, 86.7 ng/mL [95% CI, 75.2-100]; MIX geometric mean, 91.6 ng/mL [95% CI, 74.8-111.9]; and placebo geometric mean, 64.9 ng/mL [95% CI, 53-79.3]; analysis of covariance, P = .035; LGG vs placebo, P = .023; MIX vs placebo, P = .020). Use of MIX induced an increase in plasma IL-10 levels (P = .016).

    Conclusion

    Probiotics induced systemically detectable low-grade inflammation, which might explain the clinical effects of probiotics in AEDS and CMA.

  • 33.
    Wang, Hui
    et al.
    Unit for Clinical Systems Biology, Queen Silvia Children's Hospital, University of Gothenburg, Gothenburg, Sweden.
    Barrenäs, Fredrik
    Unit for Clinical Systems Biology, Queen Silvia Children's Hospital, University of Gothenburg, Gothenburg, Sweden.
    Bruhn, Sören
    Unit for Clinical Systems Biology, Queen Silvia Children's Hospital, University of Gothenburg, Gothenburg, Sweden.
    Mobini, Reza
    Unit for Clinical Systems Biology, Queen Silvia Children's Hospital, University of Gothenburg, Gothenburg, Sweden.
    Benson, Mikael
    Unit for Clinical Systems Biology, Queen Silvia Children's Hospital, University of Gothenburg, Gothenburg, Sweden.
    Increased IFN-gamma activity in seasonal allergic rhinitis is decreased by corticosteroid treatment2009Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 124, nr 6, s. 1360-1362Artikel i tidskrift (Refereegranskat)
  • 34.
    West, Christina E.
    et al.
    Umeå University, Sweden.
    Renz, Harald
    University of Marburg, Germany.
    Jenmalm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Kozyrskyj, Anita L.
    University of Alberta, Canada.
    Allen, Katrina J.
    University of Melbourne, Australia; University of Melbourne, Australia.
    Vuillermin, Peter
    Barwon Heatlh, Australia.
    Prescott, Susan L.
    University of Western Australia, Australia.
    MacKay, Charles
    Monash University, Australia.
    Salminen, Seppo
    University of Turku, Finland.
    Wong, Gary
    Chinese University of Hong Kong, Peoples R China; Chinese University of Hong Kong, Peoples R China.
    Sinn, John
    University of Sydney, Australia.
    Stokholm, Jakob
    University of Copenhagen, Denmark.
    Bisgaard, Hans
    University of Copenhagen, Denmark.
    Pawankar, Ruby
    Nippon Medical Sch, Japan.
    Noakes, Paul
    University of Western Australia, Australia.
    Kesper, Doerthe
    University of Marburg, Germany.
    Tulic, Meri
    University of Nice Sophia Antipolis, France.
    The gut microbiota and inflammatory noncommunicable diseases: Associations and potentials for gut microbiota therapies2015Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 135, nr 1Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Rapid environmental transition and modern lifestyles are likely driving changes in the biodiversity of the human gut microbiota. With clear effects on physiologic, immunologic, and metabolic processes in human health, aberrations in the gut microbiome and intestinal homeostasis have the capacity for multisystem effects. Changes in microbial composition are implicated in the increasing propensity for a broad range of inflammatory diseases, such as allergic disease, asthma, inflammatory bowel disease (IBD), obesity, and associated noncommunicable diseases (NCDs). There are also suggestive implications for neurodevelopment and mental health. These diverse multisystem influences have sparked interest in strategies that might favorably modulate the gut microbiota to reduce the risk of many NCDs. For example, specific prebiotics promote favorable intestinal colonization, and their fermented products have anti-inflammatory properties. Specific probiotics also have immunomodulatory and metabolic effects. However, when evaluated in clinical trials, the effects are variable, preliminary, or limited in magnitude. Fecal microbiota transplantation is another emerging therapy that regulates inflammation in experimental models. In human subjects it has been successfully used in cases of Clostridium difficile infection and IBD, although controlled trials are lacking for IBD. Here we discuss relationships between gut colonization and inflammatory NCDs and gut microbiota modulation strategies for their treatment and prevention.

  • 35. Williams, H
    et al.
    Robertson, C
    Stewart, A
    Ait-Khaled, N
    Anabwani, G
    Andersson, R
    Asher, I
    Beasley, R
    Björkstén, B
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Burr, M
    Clayton, T
    Crane, J
    Ellwood, P
    Keil, U
    Lai, C
    Javier, M
    Martinez, F
    Mitchell, E
    Montefort, S
    Pearce, N
    Jayant, S
    Sibbald, B
    Strachan, D
    von Mutius, E
    Weiland, SK
    Worldwide variations in the prevalence of symptoms of atopic eczema in the International Study of Asthma and Allergies in Childhood.  1999Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 103, s. 125-138Artikel i tidskrift (Refereegranskat)
  • 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
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. 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 patients2019Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 144, nr 1, s. 61-+Artikel i tidskrift (Refereegranskat)
    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.

  • 37.
    Zhang, Huan
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Nestor, Colm
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Zhao, Shuli
    Nanjing Medical University, Nanjing, China.
    Lentini, Antonio
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Bohle, Barbara
    Medical University of Vienna, Austria.
    Benson, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Wang, Hui
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Profiling of human CD4+ T-cell subsets identifies the TH2-specific noncoding RNA GATA3-AS12013Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 132, nr 4, s. 1005-1008Artikel i tidskrift (Övrigt vetenskapligt)
  • 38. Ädelroth, E
    et al.
    Rak, S
    Haahtela, T
    Aasand, G
    Rosenhall, L
    Zetterström, Olle
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för hälsa och miljö. Östergötlands Läns Landsting, Medicincentrum, Allergicentrum US.
    Byrne, A
    Champain, K
    Thirlwell, J
    Cioppa, GD
    Sandström, T
    Recombinant humanized mAb-E25, an anti-IgE mAb, in birch pollen-induced seasonal allergic rhinitis2000Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 106, nr 2, s. 253-259Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Allergic rhinitis is a common condition often requiring treatment. Objective: We evaluated whether recombinant humanized (rhu)mAb-E25, a recombinant humanized construct of a murine antibody that binds to circulating IgE, could control symptoms and reduce intake of concomitant medication in seasonal allergic rhinitis (SAR) induced by birch pollen if given subcutaneously in a dose schedule predicted to reduce serum free IgE levels below 25 ng/mL. Methods: We randomly assigned 251 adult subjects with a history of SAR and a positive skin test response to birch pollen to receive 300 mg of rhumAb-E25 or placebo given 2 or 3 times during the season, depending on baseline IgE levels. The primary efficacy variable was the subject's average daily nasal symptom severity score (sneezing, itching, runny, and stuffy nose) from diary data collected over the double-blind treatment period. Secondary efficacy variables included the average number of rescue antihistamine tablets per day, the proportion of days with any SAR medication use, and rhinoconjunctivitis-specific quality of life (QOL). Results: Significant between-treatment differences in favor of rhumAb-E25 were observed in average daily nasal symptom severity scores, the average number of tablets of rescue antihistamines per day, the proportion of days with any SAR medication use, and all domains of QOL. Serum-free IgE levels were markedly lower in rhumAb-E25-treated subjects and were associated with clinical effectiveness. Recombinant humanized mAb-E25 was well tolerated. No anti-rhumAb-E25 antibodies were detected. Conclusion: Compared with placebo, rhumAb-E25 was safe and effective in controlling birch pollen-induced SAR symptoms, with less concomitant medication use and improved QOL. This study shows the therapeutic potential of anti-IgE antibody in SAR.

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