Evidence map›Paper›PMID 28560287›Full record

ReviewCellular and molecular gastroenterology and hepatology2017

Mend Your Fences: The Epithelial Barrier and its Relationship With Mucosal Immunity in Inflammatory Bowel Disease.

Eva Martini, Susanne M Krug, Britta Siegmund, Markus F Neurath, Christoph Becker

Open access · goldAbstract readReview
In one paragraph

Review in Cellular and molecular gastroenterology and hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 362 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
362citing papers in PubMed, 2 pooled it
13.1field-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

362 citing papers in PubMed, 2 syntheses or guidelines pooled it, 664 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Antioxidants (Basel, Switzerland) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Preventive Effects ofFood science & nutrition · 2026
    Article
  15. Review
  16. Review
  17. Article
  18. METTL3 loss exacerbates colitis via mActa pharmacologica Sinica · 2026
    Article
  19. Article
  20. Article

302 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 2 institutions in 1 country.

Eva MartiniMedical Clinic 1, Friedrich-Alexander-University, Erlangen, Germany.
Susanne M KrugInstitute of Clinical Physiology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Britta SiegmundDepartment of Gastroenterology, Rheumatology and Infectious Diseases, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Markus F NeurathMedical Clinic 1, Friedrich-Alexander-University, Erlangen, Germany.
Christoph BeckerMedical Clinic 1, Friedrich-Alexander-University, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intestinal epithelium can be easily disrupted during gut inflammation as seen in inflammatory bowel disease (IBD), such as ulcerative colitis or Crohn's disease. For a long time, research into the pathophysiology of IBD has been focused on immune cell-mediated mechanisms. Recent evidence, however, suggests that the intestinal epithelium might play a major role in the development and perpetuation of IBD. It is now clear that IBD can be triggered by disturbances in epithelial barrier integrity via dysfunctions in intestinal epithelial cell-intrinsic molecular circuits that control the homeostasis, renewal, and repair of intestinal epithelial cells. The intestinal epithelium in the healthy individual represents a semi-permeable physical barrier shielding the interior of the body from invasions of pathogens on the one hand and allowing selective passage of nutrients on the other hand. However, the intestinal epithelium must be considered much more than a simple physical barrier. Instead, the epithelium is a highly dynamic tissue that responds to a plenitude of signals including the intestinal microbiota and signals from the immune system. This epithelial response to these signals regulates barrier function, the composition of the microbiota, and mucosal immune homeostasis within the lamina propria. The epithelium can thus be regarded as a translator between the microbiota and the immune system and aberrant signal transduction between the epithelium and adjacent immune cells might promote immune dysregulation in IBD. This review summarizes the important cellular and molecular barrier components of the intestinal epithelium and emphasizes the mechanisms leading to barrier dysfunction during intestinal inflammation.

Indexed as

BMP, bone morphogenic proteinCD, Crohn's diseaseFz, frizzledHD, humans α-defensinIBD, inflammatory bowel diseaseIECs, intestinal epithelial cellsIL, interleukinImmune-Epithelial CrosstalkIntestinal Epithelial BarrierIntestinal InflammationJAMs, junctional adhesion moleculesLgr5, leucine rich repeat containing G-protein coupled receptor 5MARVEL, myelin and lymphocyte and related proteins for vesicle trafficking and membrane linkMLCK, myosin light chain kinaseNFκB, nuclear factor kappa-light-chain-enhancer of activated B cellsNOD-2, nucleotide-binding oligomerization domain-containing protein 2STAT, signal transducer and activator of transcriptionTAMP, tight junction–associated MARVEL proteinTJ, tight junctionTNF, tumor necrosis factorTSLP, thymic stromal lymphopoietinUC, ulcerative colitis

Identifiers

PMID28560287
PMCPMC5439240
OpenAlexW2599036809

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.