- Paper Report
- Open Access
IL-10 promotes wirway hyperresponsiveness
- Kristen page1
© Biomed Central Ltd 2001
- Received: 21 February 2001
- Published: 18 September 2001
- Asthma, bronchial hyperresponsiveness, eosinophilia, interleukin-10
Interleukin (IL)-10, a Th2 cytokine, is increased in bronchoalveolar lavage fluid following allergen challenge, and is thought to downregulate allergic inflammation. Development of airway hyperresponsiveness (AHR) in models of asthma is thought to depend on Th2-mediated inflammation, specifically inflammation bought about by increases in IL-4, IL-5, eosinophils, and Th2 lymphocytes. The aim of this study was to compare the development of AHR in wild-type and IL-10-deficient mice in response to ragweed allergen challenge.
Allergen challenge increased AHR in wild type, but not IL-10-knockout (KO), mice. Airway constriction, measured as a marker of AHR development, also increased in wild-type but not IL-10-KO mice. Administration of recombinant IL-10 increased AHR in IL-10-KO mice. AHR was detected in severe combined immunodeficient (SCID) mice receiving mononuclear splenocytes from wild-type mice but not in those that received splenocytes from IL-10-KO mice. Ragweed challenge resulted in exaggerated airway inflammation in IL-10-KO mice compared with wild-type mice, as determined by the level of eosinophils, lymphocytes, IL-4, IL-5, and serum levels of IgA, IgG1 and IgE. This enhanced inflammation was reversed by the administration of recombinant IL-10. Taken together, these data suggest that IL-10 reduces airway inflammation but promotes AHR following ragweed allergen challenge.
Adoptive transfer, IL-10 knockout mice, allergen challenge, airway resistance and constriction management.