Evidence map›Paper›PMID 41131583›Full record

ArticleJournal of translational medicine2025

Ruminococcus torques ameliorates the inflammation bowel disease and gut barrier dysfunction by modulating gut microbiota and bile acid metabolism.

Yue Lou, Yao Lv, Xiaoxi Wang, Youyou Luo, Jingan Lou, Yu Yu, Weizhong Gu, Jindan Yu, Youhong Fang, Hong Zhao and 3 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Trial
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Yue Lou *Gastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Yao Lv *Gastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Xiaoxi WangGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Youyou LuoGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Jingan LouGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Yu YuGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Weizhong GuPathology Department, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China.
Jindan YuGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Youhong FangGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Hong ZhaoGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Kerong PengGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China.
Jie ChenGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China. 6185020@zju.edu.cn.
Yan NiGastroenterology Department, Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, 310052, China. yanni617@zju.edu.cn.ORCID 0000-0003-1779-7266

Funding

Medical Science and Technology Project of Zhejiang Province 2024KY1171National Natural Science Foundation of China 82170583National Natural Science Foundation of China 82400595National Natural Science Foundation of China U23A20167the China Crohn's & Colitis Foundation No. CCCF-QF-2022B04-4the Key R&D Program of Zhejiang 2025C02085the National Key Research and Development Program of China 2021YFC2701900
6 · The paper itself

Abstract

backgroundRecent advances in microbiome-targeted therapies have uncovered immunomodulatory bacterial taxa with strain-specific therapeutic potential; however, the microbial signatures driving exclusive enteral nutrition (EEN) efficacy, particularly protective microbiota, and their mechanistic links to therapeutic outcomes remain uncharacterized in pediatric inflammatory bowel disease (IBD). Elucidating these microbial determinants and their functional pathways is critical for advancing targeted probiotic strategies in children.

methodsA cohort of treatment-naïve pediatric Crohn's disease (CD) patients and age-matched healthy controls (HC) were enrolled. Fecal samples were collected from both HC and CD patients during active phase and remission following EEN therapy. Metagenomic sequencing, qPCR validation, and targeted bile acid (BA) analysis were conducted to identify candidate protective strains and potential impacts on BA homeostasis. Mechanistic investigations were conducted using dextran sulfate sodium (DSS)- and trinitrobenzene sulfonic acid (TNBS)-induced colitis model in male mice.

resultsThe relative abundance of Ruminococcus torques (R. torques) demonstrated significant depletion in active CD cases (p = 0.02) compared to HC, which was restored after EEN treatment at remission status (p < 0.001). Its level was negatively correlated with the disease severity index (PCDAI r=-0.64; CDEIS r=-0.70) and positively correlated with the secondary to primary BA ratio (r = 0.27). In murine models, R. torques supplementation attenuated colitis severity through enhancing epithelial integrity (claudin-3, 3.3-fold; occludin, 7.5-fold), suppressing pro-inflammatory mediators (TNF-α, -44%; IL-6, -71%), regulating BA metabolism (secondary/unconjugated BAs, 29%) and autophagy pathway (LC3-II/LC3-I ratio, -1.8-fold).

conclusionsOur findings demonstrated R. torques as a novel microbial therapeutic candidate for IBD management. The anti-colitis mechanisms involve the modulation of BA metabolic homeostasis, epithelial barrier reinforcement, and inflammation resolution.

Indexed as

Bile Acids and SaltsGastrointestinal MicrobiomeInflammatory Bowel DiseasesIntestinal MucosaRuminococcusAdolescentAnimalsChildColitisCrohn DiseaseFemaleHumansMaleMiceMice, Inbred C57BLBile Acids and SaltsBile acidsExclusive enteral nutritionGut microbiotaInflammatory bowel diseaseRuminococcus torques

Identifiers

PMID41131583
PMCPMC12548225

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Registered trials

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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.