Evidence map›Paper›PMID 30413188›Full record

ReviewJournal of biomedical science2018

Microbiota dysbiosis and barrier dysfunction in inflammatory bowel disease and colorectal cancers: exploring a common ground hypothesis.

Linda Chia-Hui Yu

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of biomedical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
233citing papers in PubMed, 3 pooled it
12.3field-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

233 citing papers in PubMed, 3 syntheses or guidelines pooled it, 388 citations in OpenAlex.

  1. Pooled it
  2. Exploring the Complex Relationship between Gut Microbiota and Risk of Colorectal Neoplasia Using Bidirectional Mendelian Randomization Analysis.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023
    Pooled it
  3. Pooled it
  4. Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Comparative Genomic and Functional Profiling of ECM-Targeting Enzymes inbioRxiv : the preprint server for biology · 2026
    Article
  17. Article
  18. Article
  19. Review
  20. Review

173 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

1 author at 1 institution in 1 country.

Linda Chia-Hui YuGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. 1, Taipei, 100, Taiwan, Republic of China. lchyu@ntu.edu.tw.ORCID http://orcid.org/0000-0003-1461-3249
National Taiwan University · TW

Funding

Ministry of Science and Technology, Taiwan 107-2320-B-002-041-MY3
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a multifactorial disease which arises as a result of the interaction of genetic, environmental, barrier and microbial factors leading to chronic inflammation in the intestine. Patients with IBD had a higher risk of developing colorectal carcinoma (CRC), of which the subset was classified as colitis-associated cancers. Genetic polymorphism of innate immune receptors had long been considered a major risk factor for IBD, and the mutations were also recently observed in CRC. Altered microbial composition (termed microbiota dybiosis) and dysfunctional gut barrier manifested by epithelial hyperpermeability and high amount of mucosa-associated bacteria were observed in IBD and CRC patients. The findings suggested that aberrant immune responses to penetrating commensal microbes may play key roles in fueling disease progression. Accumulative evidence demonstrated that mucosa-associated bacteria harbored colitogenic and protumoral properties in experimental models, supporting an active role of bacteria as pathobionts (commensal-derived opportunistic pathogens). Nevertheless, the host factors involved in bacterial dysbiosis and conversion mechanisms from lumen-dwelling commensals to mucosal pathobionts remain unclear. Based on the observation of gut leakiness in patients and the evidence of epithelial hyperpermeability prior to the onset of mucosal histopathology in colitic animals, it was postulated that the epithelial barrier dysfunction associated with mucosal enrichment of specific bacterial strains may predispose the shift to disease-associated microbiota. The speculation of leaky gut as an initiating factor for microbiota dysbiosis that eventually led to pathological consequences was proposed as the "common ground hypothesis", which will be highlighted in this review. Overall, the understanding of the core interplay between gut microbiota and epithelial barriers at early subclinical phases will shed light to novel therapeutic strategies to manage chronic inflammatory disorders and colitis-associated cancers.

Indexed as

AnimalsColorectal NeoplasmsDysbiosisGastrointestinal MicrobiomeHumansImmunity, InnateInflammatory Bowel DiseasesMicebacterial internalizationbarrier functionColitiscolorectal cancersepithelial permeabilityintestinal dysbiosis

Identifiers

PMID30413188
PMCPMC6234774
OpenAlexW2900205080

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.