Enterobacter ludwigii protects DSS-induced colitis through choline-mediated immune tolerance abstract Authors

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 lud-wigii, 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 remis-sion 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 a7nAChR-mediated retinoic acid (RA) and transforming growth factor beta (TGF-b) upregulation, resulting in protecting mice against DSS-induced colitis. This study suggests potential therapeutic approaches for inflammatory bowel diseases (IBDs).

Automated summary

This study reveals the important role of commensal intestinal bacteria E. ludwigii in regulating host immune tolerance. Choline, a metabolite of E. ludwigii, is identified to increase immune tolerance and promote Treg differentiation, suggesting potential therapeutic approaches for inflammatory bowel diseases (IBDs).