title: Helminth infection modulates the development of allergen-induced airway inflammation.
abstract: It has been proposed that infections with helminths can protect from the development of allergic diseases. However, epidemiological and experimental studies have yielded conflicting results. Therefore we investigated if an infection with Nippostrongylus brasiliensis influenced the development of allergen-induced Th2 cell responses in mice. We found a decrease in allergen-induced airway eosinophilia and Eotaxin levels in the airways when mice were infected with the helminths 8 weeks, and especially 4 weeks, but not 1 or 2 weeks before ovalbumin (OVA)-airway challenge. While OVA-specific IgG1 and IgE serum levels and cutaneous hypersensitivity reactions were not reduced by the helminth infection, there was a reduction in OVA-specific IgG1 and IgE levels in bronchoalveolar lavage fluid of mice. Suppression of allergen-induced airway eosinophilia and reduction of Eotaxin production was not observed in IL-10 deficient mice. In addition, we found that helminth-induced airway eosinophilia and Eotaxin production was strongly increased in IL-10 deficient mice infected with the helminths in comparison to control mice. Taken together, these results show that infection with N. brasiliensis suppresses the development of allergen-induced airway eosinophilia and that this effect may be mediated by IL-10. Our results support the view that helminth infections can contribute to the suppression of allergies in humans.
authors.affiliation: Center for Infectious Diseases, University of Würzburg, Röntgenring 11, 97070 Würzburg, Germany.
authors.forename: Gisela
authors.initials: G
authors.lastname: Wohlleben
authors.forename: Claudia
authors.initials: C
authors.lastname: Trujillo
authors.forename: Justus
authors.initials: J
authors.lastname: Müller
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Ritze
authors.forename: Susanne
authors.initials: S
authors.lastname: Grunewald
authors.forename: Ursula
authors.initials: U
authors.lastname: Tatsch
authors.forename: Klaus J
authors.initials: KJ
authors.lastname: Erb
mesh_terms: D000485:Allergens / Q000276:immunology*; D000707:Anaphylaxis / Q000276:immunology; D000818:Animals; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D002452:Cell Count; D002478:Cells, Cultured; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D004804:Eosinophils / Q000166:cytology; D006374:Helminthiasis, Animal / Q000150:complications / Q000276:immunology*; D007073:Immunoglobulin E / Q000032:analysis / Q000097:blood / Q000378:metabolism; D007074:Immunoglobulin G / Q000032:analysis / Q000097:blood / Q000378:metabolism; D007249:Inflammation / Q000139:chemically induced / Q000150:complications / Q000276:immunology; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism; D008198:Lymph Nodes / Q000166:cytology; D016676:Macrophages, Alveolar / Q000166:cytology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009559:Nippostrongylus / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000139:chemically induced / Q000150:complications / Q000276:immunology*; D012137:Respiratory System / Q000276:immunology; D012882:Skin Tests; D013154:Spleen / Q000166:cytology; D018418:Th2 Cells / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D014611:Vaccination
chemical_list: D000485:Allergens; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; D007074:Immunoglobulin G; D007378:Interleukins; D016753:Interleukin-10; D007073:Immunoglobulin E; D007371:Interferon-gamma; D010047:Ovalbumin