Evidence map›Paper›PMID 40082467›Full record

ArticleNPJ biofilms and microbiomes2025

Gut commensals-derived succinate impels colonic inflammation in ulcerative colitis.

Rajdeep Dalal, Srikanth Sadhu, Aashima Batra, Sandeep Goswami, Jyotsna Dandotiya, Vinayakadas K V, Rahul Yadav, Virendra Singh, Kartikey Chaturvedi, Rahul Kannan and 6 more

Abstract read
In one paragraph

Article in NPJ biofilms and microbiomes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

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  16. World journal of gastroenterology · 2025
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  19. Alistipes putredinis CCUG 45780BMC microbiology · 2025
    Article
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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

16 authors.

Rajdeep DalalCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Srikanth SadhuCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Aashima BatraDepartment of Chemistry and Centre for Advanced Studies in Chemistry, Panjab University, Chandigarh, 160014, India.
Sandeep GoswamiCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Jyotsna DandotiyaCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Vinayakadas K VCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Rahul YadavCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Virendra SinghCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Kartikey ChaturvediNon-communicable disease centre, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Rahul KannanNon-communicable disease centre, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Shakti KumarDepartment of Molecular Medicine & Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow, Uttar Pradesh, India.
Yashwant KumarNon-communicable disease centre, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Deepak Kumar RathoreCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India.
Deepak B SalunkeDepartment of Chemistry and Centre for Advanced Studies in Chemistry, Panjab University, Chandigarh, 160014, India.
Vineet AhujaDepartment of Gastroenterology, All India Institute of Medical Sciences, Ansari Nagar East, New Delhi, India.
Amit AwasthiCentre for Immunobiology and Immunotherapy, Translational Health Science and Technology Institute, NCR-Biotech Science Cluster, 3 rd Milestone, Faridabad-Gurgaon Expressway, Faridabad, 121001, Haryana, India. aawasthi@thsti.res.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gut microbiota-derived metabolites play a crucial role in modulating the inflammatory response in inflammatory bowel disease (IBD). In this study, we identify gut microbiota-derived succinate as a driver of inflammation in ulcerative colitis (UC) by activating succinate-responsive, colitogenic helper T (Th) cells that secrete interleukin (IL)-9. We demonstrate that colitis is associated with an increase in succinate-producing gut bacteria and decrease in succinate-metabolizing gut bacteria. Similarly, UC patients exhibit elevated levels of succinate-producing gut bacteria and luminal succinate. Intestinal colonization by succinate-producing gut bacteria or increased succinate availability, exacerbates colonic inflammation by activating colitogenic Th9 cells. In contrast, intestinal colonization by succinate-metabolizing gut bacteria, blocking succinate receptor signaling with an antagonist, or neutralizing IL-9 with an anti-IL-9 antibody alleviates inflammation by reducing colitogenic Th9 cells. Our findings underscore the role of gut microbiota-derived succinate in driving colitogenic Th9 cells and suggesting its potential as a therapeutic target for treating IBD.

Indexed as

BacteriaColitis, UlcerativeColonGastrointestinal MicrobiomeSuccinic AcidAnimalsFemaleHumansInflammationInterleukin-9MaleMiceMice, Inbred C57BLT-Lymphocytes, Helper-InducerInterleukin-9Succinic Acid

Identifiers

PMID40082467
PMCPMC11906746

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.