Microbial metabolite butyrate facilitates M2 macrophage polarization and function

文献类型： 外文期刊

第一作者： Ji, Jian

作者： Ji, Jian;Shu, Dingming;Wang, Jie;Luo, Chenglong;Wang, Yan;Guo, Fuyou;Zou, Xian;Lv, Xiaohui;Li, Ying;Liu, Tianfei;Qu, Hao;Ji, Jian;Shu, Dingming;Wang, Jie;Luo, Chenglong;Wang, Yan;Guo, Fuyou;Zou, Xian;Lv, Xiaohui;Li, Ying;Liu, Tianfei;Qu, Hao;Zheng, Mingzhu

作者机构：

期刊名称：SCIENTIFIC REPORTS （ 影响因子：4.379； 五年影响因子：5.133 ）

ISSN： 2045-2322

年卷期： 2016 年 6 卷

页码：

收录情况： SCI

摘要： Metabolites from intestinal microbes modulate the mucosal immune system by regulating the polarization and expansion of T cells. Whether the microbial metabolites influence macrophage polarization, however, is poorly understood. Here, we show that the large bowel microbial fermentation product, butyrate, facilitates M2 macrophage polarization, in vitro and in vivo. The supernatant from butyrate-treated M2 macrophage increased the migration and enhanced the wound closure rate of MLE-12 cells. Butyrate attenuated intestinal inflammation in mice with dextran sulfate sodium (DSS)-induced colitis, with a significant increase in colonic expression of the M2 macrophage-associated protein, Arg1. M2 macrophage treated with butyrate, had increased activation of the H3K9/STAT6 signaling pathway, suggesting a mechanism for butyrate facilitated M2 macrophage polarization. Collectively, our study indicated that commensal microbe-derived butyrate is a novel activator of STAT6-mediated transcription through H3K9 acetylation driving M2 macrophage polarization, and delineated new insights into the immune interplay underlying inflammatory bowel disease.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序