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Updated: May 15, 2025

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
Akkermansia muciniphila Protects Against Trinitrobenzene Sulfonic Acid Induced Colitis by Inhibiting IL6/STAT3
Mingshan Jiang1,2,3, Yongbin Jia1,2,3, Chunxiang Ma1,2,3
1Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Akkermansia muciniphila supplementation reduces gut inflammation by inhibiting the IL-6/STAT3 pathway. This beneficial bacterium may serve as a therapeutic for colitis by modulating inflammatory responses.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory disorder.
- Investigating the role of Akkermansia muciniphila in IBD pathogenesis is crucial.
- Understanding the link between A. muciniphila and the IL-6/STAT3 pathway is key.
Purpose of the Study:
- To explore the relationship between A. muciniphila abundance and the IL-6/STAT3 pathway.
- To elucidate the molecular mechanisms of A. muciniphila in a TNBS-induced enteritis model.
- To assess the impact of A. muciniphila on inflammatory cytokines and proteins.
Main Methods:
- Utilized mucosal biopsies and fecal samples to assess A. muciniphila levels.
- Established TNBS-induced colitis mouse models to study disease mechanisms.
- Employed 16S rRNA sequencing to analyze gut microbiota composition.
Main Results:
- A negative correlation was observed between A. muciniphila and STAT3/IL-6 levels in Crohn's disease patients.
- A. muciniphila supplementation downregulated IL-6, p-STAT3, and STAT3 expression in TNBS-induced enteritis.
- Supplementation with A. muciniphila increased gut microbial diversity and abundance.
Conclusions:
- A. muciniphila supplementation alleviates gastrointestinal inflammation via the IL-6/STAT3 pathway.
- Downregulation of IL-6 and STAT3 mediates the protective effect of A. muciniphila.
- A. muciniphila shows therapeutic potential for colitis by modulating IL-6/STAT3 signaling.
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