Evidence map›Paper›PMID 37874904›Full record

ArticleInflammatory bowel diseases2024

Dysregulated Immunity to Clostridioides difficile in IBD Patients Without a History of Recognized Infection.

Laura Cook, May Q Wong, William D Rees, Alana Schick, Daniel J Lisko, Genelle R Lunken, Xiaojiao Wang, Hannah Peters, Laura Oliveira, Torey Lau and 4 more

Abstract read
In one paragraph

Article in Inflammatory bowel diseases, 2024. 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
–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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Biomedicines · 2025
    Review
  4. Global Patterns ofCrohn's & colitis 360 · 2025
    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

14 authors.

Laura CookDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.ORCID 0000-0003-3153-2045
May Q WongDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
William D ReesDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
Alana SchickGut4Health, BC Children's Hospital Research Institute, Vancouver, BC, Canada.
Daniel J LiskoDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
Genelle R LunkenDepartment of Pediatrics, University of British Columbia, Vancouver, BC, Canada.
Xiaojiao WangDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
Hannah PetersDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
Laura OliveiraDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
Torey LauDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
Regan MahDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.
Brian BresslerGastrointestinal Research Institute, Vancouver, BC, Canada.
Megan K LevingsBC Children's Hospital Research Institute, Vancouver, BC, Canada.
Theodore S SteinerDepartment of Medicine, University of British Columbia, Vancouver, BC, Canada.

Funding

CIHR 20R76508
6 · The paper itself

Abstract

BACKGROUND &

aimsClostridioides difficile is a toxin-secreting bacteria that is an urgent antimicrobial resistance threat, with approximately 25% of patients developing recurrent infections. Inflammatory bowel disease (IBD) patients are at increased risk of severe, recurrent C. difficile infection.

methodsTo investigate a role for C. difficile infection in IBD pathogenesis, we collected peripheral blood and stool from 20 each of ulcerative colitis patients, Crohn's disease patients, and healthy control subjects. We used a flow cytometric activation induced marker assay to quantify C. difficile toxin-specific CD4+ T cells and 16S ribosomal RNA sequencing to study microbiome diversity.

resultsWe found IBD patients had significantly increased levels of C. difficile toxin B-specific CD4+ T cells, but not immunoglobulin G or immunoglobulin A, compared with healthy control subjects. Within antigen-specific CD4+ T cells, T helper type 17 cells and cells expressing the gut homing receptor integrin β7 were reduced compared with healthy control subjects, similar to our previous study of non-IBD patients with recurrent C. difficile infection. Stool microbiome analysis revealed that gut homing, toxin-specific CD4+ T cells negatively associated with microbial diversity and, along with T helper type 17 cells, positively associated with bacteria enriched in healthy control subjects.

conclusionsThese data suggest that IBD patients, potentially due to underlying intestinal dysbiosis, experience undiagnosed C. difficile infections that result in impaired toxin-specific immunity. This may contribute to the development of inflammatory T cell responses toward commensal bacteria and provide a rationale for C. difficile testing in IBD patients.

Indexed as

Bacterial ProteinsCD4-Positive T-LymphocytesClostridioides difficileClostridium InfectionsFecesGastrointestinal MicrobiomeAdultBacterial ToxinsCase-Control StudiesColitis, UlcerativeCrohn DiseaseFemaleHumansInflammatory Bowel DiseasesIntegrin beta ChainsMaleBacterial ProteinsBacterial Toxinsintegrin beta7Integrin beta ChainsRNA, Ribosomal, 16StoxB protein, Clostridium difficileantimicrobial resistanceCD4+ T cellC. difficilemicrobiomeT cell memory

Identifiers

PMID37874904
PMCPMC11063544

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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.