期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 44, 期 3, 页码 673-682出版社
WILEY
DOI: 10.1002/eji.201343717
关键词
IL-23p19; Inflammatory bowel disease; MicroRNAs; miR-107; TLR
类别
资金
- NIH [DK079918, DK098370]
- John Sealy Memorial Endowment Fund
- National Natural Science Foundation of China [81061120521, 81270470]
- Shanghai Science and Technology Commission [12XD1404000]
Commensal flora plays an important role in the development of the mucosal immune system and in maintaining intestinal homeostasis. However, the mechanisms involved in regulation of host-microbiota interaction are still not completely understood. In this study, we examined how microbiota and intestinal inflammatory conditions regulate host microRNA expression and observed lower microRNA-107 (miR-107) expression in the inflamed intestines of colitic mice, compared with that in normal control mice. miR-107 was predominantly reduced in epithelial cells and CD11c(+) myeloid cells including dendritic cells and macrophages in the inflamed intestines. We demonstrate that IL-6, IFN-, and TNF- downregulated, whereas TGF- promoted, miR-107 expression. In addition, miR-107 expression was higher in the intestines of germ-free mice than in mice housed under specific pathogen-free conditions, and the presence of microbiota downregulated miR-107 expression in DCs and macrophages in a MyD88- and NF-B-dependent manner. We determined that the ectopic expression of miR-107 specifically repressed the expression of IL-23p19, a key molecule in innate immune responses to commensal bacteria. We concluded that regulation of miR-107 by intestinal microbiota and proinflammatory cytokine serve as an important pathway for maintaining intestinal homeostasis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据