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ArticleDigestive diseases and sciences2025

Faecalibacterium prausnitzii Ameliorates DSS-Induced Colitis via Modulating Bile Acid Metabolism and Regulating FXR Signaling.

Pingnan Zhang, Saifei Xu, Na Li, Chenggong Yu

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Article in Digestive diseases and sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Pingnan ZhangDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China.
Saifei XuDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China.
Na LiDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China.
Chenggong YuDepartment of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China. chenggong_yu@nju.edu.cn.

Funding

National Natural Science Foundation of China 82170551
6 · The paper itself

Abstract

backgroundUlcerative 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.

aimsThis 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.

methodsMice 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.

resultsF. 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

conclusionThis 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.

Indexed as

Bile Acids and SaltsColitisColitis, UlcerativeFaecalibacterium prausnitziiGastrointestinal MicrobiomeReceptors, Cytoplasmic and NuclearAnimalsDextran SulfateDisease Models, AnimalMaleMiceMice, Inbred C57BLReceptor, Farnesoid X-ActivatedSignal TransductionBile Acids and SaltsDextran SulfateReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearBile acidFaecalibacterium prausnitziiFXRGut microbiotaInflammatory bowel disease

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.