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Published on: February 27, 2014
Faecalibacterium prausnitzii Ameliorates DSS-Induced Colitis via Modulating Bile Acid Metabolism and Regulating FXR
Pingnan Zhang1, Saifei Xu1, Na Li1
1Department of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China.
Background:
Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease with a globally increasing incidence. Faecalibacterium prausnitzii (F. prausnitzii) is known for its anti-inflammatory and immunomodulatory properties. However, the mechanisms by which gut microbiota and bile acid metabolism contribute to the therapeutic effects of F. prausnitzii in colitis remain unclear.
Aims:
This study aims to investigate the effects of F. prausnitzii on colitis and elucidate its potential mechanism through modulation of gut microbiota and bile acid metabolism.
Methods:
Mice were treated with dextran sulfate sodium (DSS), followed by administration of F. prausnitzii and its supernatant. Colitis symptoms, inflammatory responses, and intestinal barrier integrity were then evaluated. 16S rRNA sequencing and targeted bile acid metabolomics analysis were performed.
Results:
F. prausnitzii and its supernatant reshaped dysbiotic gut microbiota in DSS-induced colitis mouse models, increasing the ratio of unconjugated to conjugated bile acids and secondary to primary bile acids, thereby activating the farnesoid X receptor (FXR) signaling pathway. Experiments in FXR-/- mice confirmed that FXR is a critical target for the protective effects of F. prausnitzii, promoting intestinal mucosal repair and inhibiting NLRP3 inflammasome activation, which in turn alleviates colitis. Additionally, the differential bile acid isoLCA, enriched by F. prausnitzii and its supernatant, effectively suppressed inflammation and enhanced intestinal barrier function.
Conclusion:
This study demonstrates that F. prausnitzii alleviates colitis by modulating bile acid composition and regulating FXR signaling, suggesting that targeting the microbiota-bile acid-FXR pathway may represent a promising therapeutic strategy for inflammatory bowel disease.
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