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Critical role of interleukin-5 in the development of a mite antigen-induced chronic bronchial asthma model

Objective and design Asthma is associated with eosinophilic airway inflammation and characterized by enhanced airway sensitivity. Interleukin (IL)-5 plays an important role in the pathogenesis of asthma. The involvement of IL-5 receptor-mediated cellular signals in the pathogenesis of a mite antigen...

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Published in:Inflammation research 2013-10, Vol.62 (10), p.911-917
Main Authors: Shimizu, Hiroki, Obase, Yasushi, Katoh, Shigeki, Mouri, Keiji, Kobashi, Yoshihiro, Oka, Mikio
Format: Article
Language:English
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Summary:Objective and design Asthma is associated with eosinophilic airway inflammation and characterized by enhanced airway sensitivity. Interleukin (IL)-5 plays an important role in the pathogenesis of asthma. The involvement of IL-5 receptor-mediated cellular signals in the pathogenesis of a mite antigen-induced chronic asthma model was investigated. Subjects In this study, 48 female C57BL/6J (WT) mice and IL-5 receptor-deficient (IL-5RKO) mice were used. Treatment Mite antigen (50 μl) was intranasally administered 13 times to WT and IL-5RKO mice. Methods Airway hypersensitivity (Mch PC 200 ) and specific antigen exposure tests were performed, and lung tissue, bronchoalveolar lavage fluid (BALF), and blood were collected to investigate the asthma pathology and differences in the local pulmonary levels of cytokines and chemokines. Results Airway sensitivity was enhanced and antigen-specific airway resistance was increased in WT mice. In addition, the number of eosinophils and Th2 cytokine levels in the BALF were increased. In contrast, IL-5RKO mice did not acquire the asthma pathology, such as antigen-specific airway resistance and eosinophilic airway inflammation. Mch PC 200 was significantly correlated with cysteinyl leukotriene levels in WT mice. Conclusion These findings suggested that both IL-5 induced eosinophils and cysteinyl leukotrienes are involved in the pathology of this mite antigen-induced chronic asthma model.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-013-0651-y