Evidence map›Paper›PMID 40022210›Full record

ArticleMicrobiome2025

Enterocloster clostridioformis protects against Salmonella pathogenesis and modulates epithelial and mucosal immune function.

Benjamin S Beresford-Jones, Satoshi Suyama, Simon Clare, Amelia Soderholm, Wangmingyu Xia, Puspendu Sardar, Junhee Lee, Katherine Harcourt, Trevor D Lawley, Virginia A Pedicord

Abstract read
In one paragraph

Article in Microbiome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Frontiers in microbiology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
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

10 authors.

Benjamin S Beresford-JonesJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Satoshi SuyamaJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Simon ClareJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Amelia SoderholmJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Wangmingyu XiaJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Puspendu SardarJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Junhee LeeJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Katherine HarcourtJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK.
Trevor D LawleyWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, UK.
Virginia A PedicordJeffrey Cheah Biomedical Centre, Cambridge Institute of Therapeutic Immunology and Infectious Disease, Cambridge Biomedical Campus, Cambridge, UK. vap33@cam.ac.uk.

Funding

Rosetrees Trust A2194Rosetrees Trust PGS22/100116Wellcome TrustWellcome Trust 098051Wellcome Trust 206245/Z/17/Z
6 · The paper itself

Abstract

backgroundPromoting resistance to enteric pathogen infection is a core function of the gut microbiota; however, many of the specific host-commensal interactions that mediate this protection remain uncharacterised. To address this knowledge gap, we monocolonised germ-free mice with mouse-derived commensal microbes to screen for microbiota-induced resistance to Salmonella Typhimurium infection.

resultsWe identified Enterocloster clostridioformis as a protective species against S. Typhimurium infection. E. clostridioformis selectively upregulates resistin-like molecule β and cell cycle pathway expression at the level of caecal epithelial cells and increases T-regulatory cells in the underlying mucosal immune system, potentially contributing to reduced infection-induced pathology.

conclusionsWe highlight novel mechanisms of host-microbe interactions that can mediate microbiota-induced resistance to acute salmonellosis. In the backdrop of increasing antibiotic resistance, this study identifies novel potential avenues for further research into protective host responses against enteric infections and could lead to new therapeutic approaches. Video Abstract.

Indexed as

Gastrointestinal MicrobiomeImmunity, MucosalIntestinal MucosaSalmonella InfectionsSalmonella typhimuriumAnimalsCecumEpithelial CellsHost Microbial InteractionsHost-Pathogen InteractionsMiceMice, Inbred C57BLT-Lymphocytes, RegulatoryAcute salmonellosisEnterocloster clostridioformisEscherichia coliHost–commensal interactionsMicrobiotaMouse modelsPathogen resistanceResistin-like molecule βScreenT-regulatory cells

Identifiers

PMID40022210
PMCPMC11869688

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.