结肠炎
免疫系统
免疫耐受
维甲酸
化学
肠杆菌
微生物学
免疫学
生物
大肠杆菌
生物化学
基因
作者
Qianqian Li,Xuan Sun,Kaiyuan Yu,Junqiang Lv,Chunhui Miao,Jianming Yang,Song Wang,Zheng Fu,Yamin Sun,Hong Zhang,Zhi‐Song Zhang,Evan T. Keller,Zhi Yao,Quan Wang
出处
期刊:Cell Reports
[Cell Press]
日期:2022-08-01
卷期号:40 (9): 111308-111308
被引量:28
标识
DOI:10.1016/j.celrep.2022.111308
摘要
Commensal intestinal bacteria play key roles in regulating host immune tolerance; however, bacterial strains and related metabolites directly involved in this regulation are largely unknown. Here, using a mouse model of dextran sulfate sodium (DSS)-induced colitis combined with different antibiotic treatment, Enterobacter ludwigii, abundant in microbiota of mice treated with metronidazole, is screened out to have prophylactic and therapeutic effects on DSS-induced colitis with or without the presence of complex intestinal bacteria. E. ludwigii is found to induce CD103+DC and regulatory T (Treg)-mediated immune tolerance for colitis remission using in vitro and in vivo experiments. Moreover, choline, one metabolite of E. ludwigii, is identified to increase dendritic cells' (DCs) immune tolerance to promote Treg differentiation. E. ludwigii is found to induce DCs' immune tolerance ability for Treg differentiation through choline and α7nAChR-mediated retinoic acid (RA) and transforming growth factor beta (TGF-β) upregulation, resulting in protecting mice against DSS-induced colitis. This study suggests potential therapeutic approaches for inflammatory bowel diseases (IBDs).
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