Evidence map›Paper›PMID 35862710›Full record

ArticleInfection and immunity2022

Tauroursodeoxycholic Acid Inhibits Clostridioides difficile Toxin-Induced Apoptosis.

Colleen M Pike, John Tam, Roman A Melnyk, Casey M Theriot

Open access · hybridAbstract read
In one paragraph

Article in Infection and immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 15% of its field
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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Dietary iron attenuatesVirulence · 2025
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  4. Effects of Bile on PathogenicBiomolecules · 2025
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  5. Unravelling three-way interactions betweenJournal of medical microbiology · 2025
    Review
  6. Infection and immunity · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. The microbial derived bile acid lithocholate and its epimers inhibitbioRxiv : the preprint server for biology · 2023
    Article
  11. Intestinal bile acids provide a surmountable barrier againstProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Review
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

4 authors at 3 institutions in 2 countries.

Colleen M PikeDepartment of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State Universitygrid.40803.3f, Raleigh, North Carolina, USA.
John TamMolecular Medicine, Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada.
Roman A MelnykMolecular Medicine, Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada.ORCID 0000-0002-7187-2362
Casey M TheriotDepartment of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State Universitygrid.40803.3f, Raleigh, North Carolina, USA.ORCID 0000-0002-1895-8941
North Carolina State University · USHospital for Sick Children · CAUniversity of Toronto · CA

Funding

Targeted bacterial restoration of colonization resistance against C. difficileR35GM119438 · NIGMS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI THERIOT, CASEY MICHELLE · 2016 to 2020
$1.6M
HHS | NIH | National Institute of General Medical Sciences (NIGMS) R35GM119438NIGMS NIH HHS R35 GM119438
6 · The paper itself

Abstract

C. difficile infection (CDI) is a highly inflammatory disease mediated by the production of two large toxins that weaken the intestinal epithelium and cause extensive colonic tissue damage. Antibiotic alternative therapies for CDI are urgently needed as current antibiotic regimens prolong the perturbation of the microbiota and lead to high disease recurrence rates. Inflammation is more closely correlated with CDI severity than bacterial burden, thus therapies that target the host response represent a promising yet unexplored strategy for treating CDI. Intestinal bile acids are key regulators of gut physiology that exert cytoprotective roles in cellular stress, inflammation, and barrier integrity, yet the dynamics between bile acids and host cellular processes during CDI have not been investigated. Here we show that several bile acids are protective against apoptosis caused by C. difficile toxins in Caco-2 cells and that protection is dependent on conjugation of bile acids. Out of 20 tested bile acids, taurine conjugated ursodeoxycholic acid (TUDCA) was the most potent inhibitor, yet unconjugated UDCA did not alter toxin-induced apoptosis. TUDCA treatment decreased expression of genes in lysosome associated and cytokine signaling pathways. TUDCA did not affect C. difficile growth or toxin activity

Indexed as

Clostridioides difficileClostridium InfectionsAnti-Bacterial AgentsAntibodies, BacterialApoptosisBile Acids and SaltsCaco-2 CellsHumansInflammationTaurochenodeoxycholic AcidUrsodeoxycholic AcidAnti-Bacterial AgentsAntibodies, BacterialBile Acids and SaltsTaurochenodeoxycholic AcidUrsodeoxycholic Acidursodoxicoltaurineapoptosisbile acidsClostridioides difficiletauroursodeoxycholic acidtoxinursodeoxycholic acid

Identifiers

PMID35862710
PMCPMC9387233
OpenAlexW4284887384

What OpenQuestion 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 OpenQuestion graph.