Evidence map›Paper›PMID 42191723›Full record

ArticleNPJ science of food2026

Eubacterium rectale Mitigates Inflammatory Bowel Disease via Modulation of Glutamine Metabolism Through the GLS2 and NF-κB Pathway.

Lu Han, Yiyi Jin, Wen Lin, Zide Liu, Chunyan Zeng, Youxiang Chen

Abstract read
In one paragraph

Article in NPJ science of food, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Lu Han *Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Yiyi Jin *Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Wen Lin *Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Zide LiuDepartment of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Chunyan ZengDepartment of Gastroenterology, Jiangxi Province Hospital of Integrated Chinese and Western Medicine, Nanchang, Jiangxi, China. chunyanzeng@163.com.
Youxiang ChenDepartment of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. chenyx102@ncu.edu.cn.

Funding

Jiangxi Provincial Traditional Chinese Medicine Administration Science and Technology Plan Project 2024A0032the Foundation of Jiangxi Provincial Department of Science and Technology 20252BAC240418the Jiangxi Provincial Natural Science Foundation 20232BAB216018the National Natural Science Foundation of China 82360112
6 · The paper itself

Abstract

Inflammatory Bowel Disease (IBD) is a chronic inflammatory intestinal disorder with complex etiology, closely associated with gut microbiota dysbiosis. This study demonstrates that Eubacterium rectale (ER), a beneficial commensal bacterium, alleviates dextran sulfate sodium (DSS)-induced colitis in mice, as evidenced by improved clinical symptoms, restored intestinal barrier integrity, and reduced pro-inflammatory cytokine levels. Mechanistic investigations revealed that ER specifically upregulates the expression of glutaminase 2 (GLS2), ameliorates DSS-induced disturbances in glutamine (Gln) metabolism within intestinal epithelial cells, and subsequently inhibits the NF-κB signaling pathway to exert anti-inflammatory effects. Further validation showed that GLS2 deficiency abolishes the anti-inflammatory effects of ER. Collectively, this work identifies a therapeutically relevant mechanism: ER mitigates colitis via the GLS2/NF-κB axis. These insights pave the way for developing ER-derived live biotherapeutic products for IBD.

Identifiers

PMID42191723
PMCPMC13482563

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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.