Abstract
Abstract BACKGROUND: Asthma is a chronic inflammatory disorder of the airways. Recently, IL-22 has been shown to mediate unclear anti-inflammatory effects in mouse models of lung inflammations. OBJECTIVE: To investigate the anti-inflammatory role of IL-22 in human asthma. METHODS: T cells derived from lung biopsies of asthmatic patients were characterized by flow cytometry. Human bronchial epithelial cells were stimulated with IL-22, IFNg or the combination of both cytokines, and their effects were investigated by whole genome analysis, ELISA and flow cytometry. The functional consequence of cytokine effects was evaluated by in vitro wound repair and T cell mediated cytotoxicity experiments. In vivo cytokine expression was measured by luminex in bronchioalveolar lavage fluids (BAL) of asthmatic patients. RESULTS: Th22 produce IL-22 during asthma. IFNg and IL-22 induced antagonistic responses on epithelial cells. IFNg antagonized IL-22 mediated wound closure while IL-22 impaired the expression of IFNg induced molecules such as MHC-I, MHC-II, CD54/ICAM-1, CCL5/RANTES, CXCL10/IP-10 and the CD8-mediated epithelial cell damage. Consistently, the IL22/IFNg ratio inversely correlated with the expression of CCL5/RANTES and CXCL10/IP-10 in BAL fluids of asthmatic patients. CONCLUSIONS: IL-22 is the first cytokine that act as anti-inflammatory by inhibiting IFNg pro-inflammatory effects on epithelial cells. IL-22 might be used to control the extent of IFNg mediated lung inflammation.
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