Enterobacter ludwigii protects DSS-induced colitis through choline-mediated immune tolerance.
Cell Rep
; 40(9): 111308, 2022 08 30.
Article
en En
| MEDLINE
| ID: mdl-36044853
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-ß) upregulation, resulting in protecting mice against DSS-induced colitis. This study suggests potential therapeutic approaches for inflammatory bowel diseases (IBDs).
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Colina
/
Colitis
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Cell Rep
Año:
2022
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Estados Unidos