Attenuation of allergic airway inflammation in IL-4 deficient mice
Autor: | Claude Cuvelier, J Van der Heyden, Romain Pauwels, Guy Brusselle, Horst Bluethmann, Johan Kips, Jan Tavernier |
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Rok vydání: | 1994 |
Předmět: |
Allergy
Pathology medicine.medical_specialty medicine.medical_treatment T cell Immunology Inflammation Mice Eosinophilia medicine Animals Immunology and Allergy Lymphocytes Mast Cells Bronchitis Lung biology business.industry Histocompatibility Antigens Class II Immunoglobulin E respiratory system Eosinophil medicine.disease Mast cell Asthma Mice Mutant Strains Specific Pathogen-Free Organisms respiratory tract diseases Eosinophils Mice Inbred C57BL Disease Models Animal Ovalbumin medicine.anatomical_structure Cytokine biology.protein Female Interleukin-4 medicine.symptom business Bronchoalveolar Lavage Fluid |
Zdroj: | Europe PubMed Central |
ISSN: | 1365-2222 0954-7894 |
Popis: | To investigate the role of IL-4 in vivo in allergic asthma, we developed a murine model of allergen-induced airway inflammation. Repeated daily exposures of actively immunized C57BL/6 mice to aerosolized ovalbumin (OVA) induced a peribronchial inflammation and an increase in eosinophils and lymphocytes in bronchoalveolar-lavage (BAL) fluid. In IL-4 deficient (IL4-/-) mice, treated in the same way, there were substantially fewer eosinophils in BAL and much less peribronchial inflammation compared with wild type mice. In this model, mast cell deficient (W/Wv) mice developed a similar degree of BAL eosinophilia and peribronchial inflammation as wild type mice, demonstrating that the mast cell is not required for the induction of chronic airway inflammation. In contrast, BAL eosinophilia and airway inflammation were absent in OVA-treated MHC ClassII deficient (B6.Aa-/-) mice which lack mature CD4+ T lymphocytes. In conclusion, these results indicate that IL-4 is a central mediator of allergic airway inflammation, regulating antigen-induced eosinophil recruitment into the airways by a T cell dependent mechanism. |
Databáze: | OpenAIRE |
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