Evidence map›Paper›PMID 35185922›Full record

ReviewFrontiers in immunology2022

The Emerging Role of Bile Acids in the Pathogenesis of Inflammatory Bowel Disease.

John P Thomas, Dezso Modos, Simon M Rushbrook, Nick Powell, Tamas Korcsmaros

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
11.2field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. mSystems · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Luohuazizhu Granules Alleviate Symptoms of Ulcerative ColitisCombinatorial chemistry & high throughput screening · 2026
    Article
  17. Review
  18. Ornithine lipids fromGut microbes · 2025
    Article
  19. Review
  20. Article

38 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

John P ThomasGut Microbes and Health Programme, Quadram Bioscience, Norwich, United Kingdom.
Dezso ModosGut Microbes and Health Programme, Quadram Bioscience, Norwich, United Kingdom.
Simon M RushbrookGut Microbes and Health Programme, Quadram Bioscience, Norwich, United Kingdom.
Nick PowellDivision of Digestive Diseases, Imperial College London, London, United Kingdom.
Tamas KorcsmarosGut Microbes and Health Programme, Quadram Bioscience, Norwich, United Kingdom.
Quadram Institute · GBEarlham Institute · GBImperial College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/CSP1720/1Biotechnology and Biological Sciences Research Council BB/R012490/1Biotechnology and Biological Sciences Research Council BBS/E/F/000PR10353Biotechnology and Biological Sciences Research Council BBS/E/F/000PR10355Biotechnology and Biological Sciences Research Council BBS/E/T/000PR9817Biotechnology and Biological Sciences Research Council BBS/E/T/000PR9819Department of Health
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a chronic immune-mediated inflammatory disorder of the gastrointestinal tract that arises due to complex interactions between host genetic risk factors, environmental factors, and a dysbiotic gut microbiota. Although metagenomic approaches have attempted to characterise the dysbiosis occurring in IBD, the precise mechanistic pathways interlinking the gut microbiota and the intestinal mucosa are still yet to be unravelled. To deconvolute these complex interactions, a more reductionist approach involving microbial metabolites has been suggested. Bile acids have emerged as a key class of microbiota-associated metabolites that are perturbed in IBD patients. In recent years, metabolomics studies have revealed a consistent defect in bile acid metabolism with an increase in primary bile acids and a reduction in secondary bile acids in IBD patients. This review explores the evolving evidence that specific bile acid metabolites interact with intestinal epithelial and immune cells to contribute to the inflammatory milieu seen in IBD. Furthermore, we summarise evidence linking bile acids with intracellular pathways that are known to be relevant in IBD including autophagy, apoptosis, and the inflammasome pathway. Finally, we discuss how novel experimental and bioinformatics approaches could further advance our understanding of the role of bile acids and inform novel therapeutic strategies in IBD.

Indexed as

AnimalsBile Acids and SaltsDysbiosisGastrointestinal MicrobiomeHumansInflammatory Bowel DiseasesIntestinal MucosaBile Acids and Saltsbile acidsCrohn’s diseasegut metabolitesgut microbiomeimmunology and inflammationinflammatory bowel diseaseulcerative colitis

Identifiers

PMID35185922
PMCPMC8850271
OpenAlexW4213270373

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.