期刊
MOLECULAR THERAPY-NUCLEIC ACIDS
卷 30, 期 -, 页码 208-225出版社
CELL PRESS
DOI: 10.1016/j.omtn.2022.09.018
关键词
-
资金
- National Natural Science Foundation of China
- National Key R&D Program of China
- Fundamental Research Funds for the Central Universities
- Key Program for Science & Tech- nology from Henan Education Department
- [81970726]
- [81472232]
- [2021YFC2103900]
- [PT2001]
- [21A310001]
Deletion of miR-149-3p increases susceptibility to colitis and alters inflammatory cytokine expression, while miR-149-5p and miR-149-3p can suppress colon inflammatory response. Furthermore, deletion of miR-149-3p alters gut microbiota composition.
Genetic predisposition and disruption of host gut microbiota and immune system can result in inflammatory bowel disease (IBD). Here, we show that miRNA-149-5p (miR-149-5p) and miRNA-149-3p (miR-149-3p) play crucial roles in IBD. Mice lacking miR-149-3p were considerably more susceptible to dextran sulfate sodium (DSS)-induced colitis than wild-type (WT) mice, accompanied by more serious inflammatory symp-toms and increased gene expression of certain inflammatory cytokines. Both miR-149-5p and miR-149-3p suppressed colon inflammatory response in vitro and in vivo. Furthermore, we found significant differences in the composition of the gut mi-crobiota between WT and miR-149-3p-/-mice by 16S rRNA sequencing. Co-housing endowed susceptibility to WT mice against DSS-induced colitis compared with the WT control group. However, susceptibility of miR-149-3p-/-mice against DSS-induced colitis was still present after antibiotic treatment. These findings suggest that the deletion of miR-149-3p altered gut microbiota and influenced pathogenesis of intestinal inflammation, but sensitivity of miR-149-3p-/-mice to DSS-induced colitis is not conferred by microbiota. In addition, we identified the roles of miR-149-5p and miR-149-3p in colon inflammation, which may serve as an attractive therapeutic tool for colitis or IBD, and even colitis-associated carcinoma.
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