Allergen-induced airway inflammation and bronchial responsiveness in interleukin-5 receptor alpha chain-deficient mice

Objective The role of IL-5 receptor alpha chain (IL-5R alpha) in the onset of bronchial hyperresponsiveness (BHR) to acetylcholine was investigated by testing IL-5R alpha knockout (IL-5R alpha 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 thre e times every fourth day. Twenty-four hours after the last antigen challeng e, bronchial responsiveness to acetylcholine was measured and bronchoalveol ar lavage was carried out. Results Twenty-four hours after the last antigen inhalation, total and diff erential cells counts of bronchoalveolar lavage revealed a significant incr ease in eosinophils and lymphocytes in ovalbumin-exposed wild-type mice. In IL-5R alpha KO mice, there was little increase of eosinophils in bronchoal veolar lavage fluid (BALF). The production of IL-5 in BALF increased in bot h mice after repeated antigen challenge, and there was no significant diffe rence between wild-type and IL-5R alpha 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 def iciency of IL-5R alpha chain. There was no significant difference in serum antigen-specific IgE levels between wild-type and IL-5R alpha KO mice after immunization nor antigen inhalation. Repeated antigen provocation caused B HR to acetylcholine in wild-type mice. In contrast, no BHR was observed in IL-5R alpha KO mice after repeated inhalation of antigen. Conclusion These findings indicate that IL-5R alpha plays an important role in the development of antigen-induced airway eosinophilia and BHR in mice.