Evidence map›Paper›PMID 37822139›Full record

ReviewGut microbes2023

Current insights on the roles of gut microbiota in inflammatory bowel disease-associated extra-intestinal manifestations: pathophysiology and therapeutic targets.

Yizhe Tie, Yongle Huang, Rirong Chen, Li Li, Minhu Chen, Shenghong Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Gut microbes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
10.8field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. TibetanNutrients · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Effect ofTherapeutic advances in gastroenterology · 2026
    Review
  15. Article
  16. Review
  17. Article
  18. Reduced gut microbial diversity characterized by decreasedFrontiers in cellular and infection microbiology · 2026
    Observational
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Yizhe TieDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Yongle HuangDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Rirong ChenDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Li LiDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Minhu ChenDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Shenghong ZhangDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0002-9088-8781
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a chronic, recurrent inflammatory disease of the gastrointestinal tract. In addition to digestive symptoms, patients with IBD may also develop extra-intestinal manifestations (EIMs), the etiology of which remains undefined. The gut microbiota has been reported to exert a critical role in the pathogenesis of IBD, with a similar pattern of gut dysbiosis observed between patients with IBD and those with EIMs. Therefore, it is hypothesized that the gut microbiota is also involved in the pathogenesis of EIMs. The potential mechanisms are presented in this review, including: 1) impaired gut barrier: dysbiosis induces pore formation in the intestinal epithelium, and activates pattern recognition receptors to promote local inflammation; 2) microbial translocation: intestinal pathogens, antigens, and toxins translocate via the impaired gut barrier into extra-intestinal sites; 3) molecular mimicry: certain microbial antigens share similar epitopes with self-antigens, inducing inflammatory responses targeting extra-intestinal tissues; 4) microbiota-related metabolites: dysbiosis results in the dysregulation of microbiota-related metabolites, which could modulate the differentiation of lymphocytes and cytokine production; 5) immunocytes and cytokines: immunocytes are over-activated and pro-inflammatory cytokines are excessively released. Additionally, we summarize microbiota-related therapies, including probiotics, prebiotics, postbiotics, antibiotics, and fecal microbiota transplantation, to promote better clinical management of IBD-associated EIMs.

Indexed as

Gastrointestinal MicrobiomeInflammatory Bowel DiseasesMicrobiotaCytokinesDysbiosisFecal Microbiota TransplantationHumansCytokinescytokineextra-intestinal manifestationgut barriergut microbiotaimmunocyteInflammatory bowel diseasemetabolitemolecular mimicrytranslocation

Identifiers

PMID37822139
PMCPMC10572083
OpenAlexW4387562943

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.