Downregulation of micro‐107 in intestinal 11c⁺ myeloid cells in response to microbiota and proinflammatory cytokines increases ‐23p19 expression

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 micro expression and observed lower micro‐107 (mi‐107) expression in the inflamed intestines of colitic mice, compared with that in normal control mice. mi‐107 was predominantly reduced in epithelial cells and 11c myeloid cells including dendritic cells and macrophages in the inflamed intestines. We demonstrate that ‐6, ‐γ, and ‐α downregulated, whereas ‐β promoted, mi‐107 expression. In addition, mi‐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 mi‐107 expression in s and macrophages in a y88‐ and ‐κB‐dependent manner. We determined that the ectopic expression of mi‐107 specifically repressed the expression of ‐23p19, a key molecule in innate immune responses to commensal bacteria. We concluded that regulation of mi‐107 by intestinal microbiota and proinflammatory cytokine serve as an important pathway for maintaining intestinal homeostasis.

Duke Scholars

Author Eric D. Carlsen Pathology