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IL-17-Producing Alveolar Macrophages Mediate Allergic Lung Inflammation Related to Asthma
Update time:2012-02-29 09:53:55   【 Font: Large  Medium Small

IL-17 is a pivotal proinflammatory molecule in asthmatics. However, the cellular source of IL-17 in asthma has not been identified to date. In this study, we report that macrophages rather than Th17 cells are the main producer of IL-17 in allergic inflammation related to asthma. After OVA challenge in a mouse model mimicking allergic asthma, the increased IL-17 cells in the lung were mainly CD11bF4/80 macrophages, instead of T cells or others. Importantly, IL-17 alveolar macrophages (AMs), but not IL-17 interstitial macrophages, were significantly increased after allergen challenge. The increase of IL-17 AMs was not due to the influx of IL-17 macrophages from circulation or other tissues, but ascribed to the activation of AMs by mediator(s) secreted by IgE/OVA-activated mast cells. Depleting alveolar macrophages or neutralizing IL-17 prevented the initiation of OVA-induced asthma-related inflammation by inhibiting the increase of inflammatory cells and inflammatory factors in bronchoalveolar lavage fluid. Th2 cytokine IL-10 could down-regulate IL-17 expression in alveolar macrophages. The increased IL-17 and the decreased IL-10 in bronchoalveolar lavage fluid were further confirmed in asthmatic patients. These findings suggest that IL-17 is mainly produced by macrophages but not Th17 cells in allergic inflammation related to asthma. Mast cell-released mediators up-regulate the expression of IL-17 by macrophages, whereas IL-10 down-regulates IL-17 expression. 

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Source:The Journal of Immunology      by Chuanwang Song,, Liqiong Luo,, Zhang Lei Bo Li, Zhihui Liang, Guanghui Liu, Dong Li, Guimei Zhang, Bo Huang, and Zuo-Hua Feng,
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