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Allergen‐induced airway inflammation and bronchial responsiveness in interleukin‐5 receptor α chain‐deficient mice
Author(s) -
Hiroyuki Tanaka,
Naoki Kawada,
Takayuki Yamada,
Kenji Kawada,
Kiyoshi Takatsu,
Hiroichi Nagai
Publication year - 2000
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2000.00828.x
Subject(s) - bronchoalveolar lavage , ovalbumin , immunology , bronchial hyperresponsiveness , medicine , antigen , eosinophilia , inhalation , interleukin 5 , immunoglobulin e , interleukin , lung , cytokine , respiratory disease , antibody , anatomy
Objective The role of IL‐5 receptor α chain (IL‐5Rα) in the onset of bronchial hyperresponsiveness (BHR) to acetylcholine was investigated by testing IL‐5Rα knockout (IL‐5Rα KO) mice. Methods Mice were immunized with antigen at intervals of 12 days. Starting 10 days after the secondary immunization, mice were exposed to antigen three times every fourth day. Twenty‐four hours after the last antigen challenge, bronchial responsiveness to acetylcholine was measured and bronchoalveolar lavage was carried out. Results Twenty‐four hours after the last antigen inhalation, total and differential cells counts of bronchoalveolar lavage revealed a significant increase in eosinophils and lymphocytes in ovalbumin‐exposed wild‐type mice. In IL‐5Rα KO mice, there was little increase of eosinophils in bronchoalveolar lavage fluid (BALF). The production of IL‐5 in BALF increased in both mice after repeated antigen challenge, and there was no significant difference between wild‐type and IL‐5Rα KO mice. Similar to the BAL study, histological sections of lung tissue from ovalbumin‐exposed wild‐type mice exhibited airway eosinophilic inflammation, which was attenuated by the deficiency of IL‐5Rα chain. There was no significant difference in serum antigen‐specific IgE levels between wild‐type and IL‐5Rα KO mice after immunization nor antigen inhalation. Repeated antigen provocation caused BHR to acetylcholine in wild‐type mice. In contrast, no BHR was observed in IL‐5Rα KO mice after repeated inhalation of antigen. Conclusion These findings indicate that IL‐5Rα plays an important role in the development of antigen‐induced airway eosinophilia and BHR in mice.