title: Allergen-induced airway inflammation and bronchial responsiveness in interleukin-5 receptor alpha chain-deficient mice.
abstract: OBJECTIVE
  The role of IL-5 receptor alpha chain (IL-5Ralpha) in the onset of bronchial hyperresponsiveness (BHR) to acetylcholine was investigated by testing IL-5Ralpha knockout (IL-5Ralpha 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-5Ralpha 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-5Ralpha 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-5Ralpha chain. There was no significant difference in serum antigen-specific IgE levels between wild-type and IL-5Ralpha 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-5Ralpha KO mice after repeated inhalation of antigen.
  
  
  CONCLUSIONS
  These findings indicate that IL-5Ralpha plays an important role in the development of antigen-induced airway eosinophilia and BHR in mice.
authors.affiliation: Department of Pharmacology, Gifu Pharmaceutical University, Gifu College of Medical Technology, Gifu, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: N
authors.initials: N
authors.lastname: Kawada
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: K
authors.initials: K
authors.lastname: Kawada
authors.forename: K
authors.initials: K
authors.lastname: Takatsu
authors.forename: H
authors.initials: H
authors.lastname: Nagai
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000485:Allergens / Q000276:immunology*; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000276:immunology*; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D004804:Eosinophils / Q000276:immunology*; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D010047:Ovalbumin / Q000008:administration & dosage / Q000009:adverse effects; D018123:Receptors, Interleukin / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D053649:Receptors, Interleukin-5
chemical_list: D000485:Allergens; D018123:Receptors, Interleukin; D053649:Receptors, Interleukin-5; D007073:Immunoglobulin E; D010047:Ovalbumin; D000109:Acetylcholine