Evidence map›Paper›PMID 23160753›Full record

ReviewLangenbeck's archives of surgery2013

Inflammatory bowel disease: an impaired barrier disease.

Simon Jäger, Eduard F Stange, Jan Wehkamp

Abstract readReview
PubMed Publisher
In one paragraph

Review in Langenbeck's archives of surgery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 133 citations in OpenAlex.

  1. Role of TRPV4 in the Diagnosis and Treatment ofBioMed research international · 2022
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  18. Exploring the Early Phase of Crohn's Disease.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2021
    Review
  19. Trace Element Selenium Effectively Alleviates Intestinal Diseases.International journal of molecular sciences · 2021
    Review
  20. Article
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

3 authors at 1 institution in 1 country.

Simon JägerDepartment of Internal Medicine I, Robert Bosch Hospital, 70376 Stuttgart, Germany.
Eduard F Stange
Jan Wehkamp
Robert Bosch Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe intestinal barrier is a delicate structure composed of a single layer of epithelial cells, the mucus, commensal bacteria, immune cells, and antibodies. Furthermore, a wealth of antimicrobial peptides (AMPs) can be found in the mucus and defend the mucosa. Different lines of investigations now point to a prominent pathophysiological role of defensins, an important family of AMPs, in the pathogenesis of inflammatory bowel disease and, particularly, in small intestinal Crohn's disease. PURPOSE: In this review, we introduce the different antimicrobial peptides of the intestinal mucosa and describe their function, their expression pattern along the gastrointestinal tract, and their spatial relationship to the mucus layer. We then focus on the alterations found in inflammatory bowel disease. Small intestinal Crohn's disease (CD) is closely linked to defects in Paneth cells (specialized secretory epithelial cells at the bottom crypts) which secrete α-defensin human defensin (HD)-5 in huge quantities in healthy individuals. Decreased expression of these antimicrobial peptides is found in ileal CD, and single nucleotide polymorphisms with the highest linkage to CD affect genes involved in Paneth cell biology and defensin secretion. Additionally, antimicrobial peptides have a role in ulcerative colitis, where the depleted mucus layer cannot fulfill its crucial function of binding defensins and other AMPs to their proper site of action.

conclusionInflammatory bowel disease arises when the mucosal barrier is compromised in its defense against challenges from the intestinal microbiota. In ileal CD, a strong association can be found between diminished expression or defective function of defensins and the advent of intestinal inflammation.

Indexed as

Antimicrobial Cationic PeptidesColitis, UlcerativeCrohn DiseaseDefensinsDNA Mutational AnalysisGenetic Predisposition to DiseaseHumansImmunity, InnateImmunogeneticsIntermediate-Conductance Calcium-Activated Potassium ChannelsIntestinal MucosaIntestine, LargeIntestine, SmallNod2 Signaling Adaptor ProteinPaneth CellsPouchitisAntimicrobial Cationic PeptidesDefensinsIntermediate-Conductance Calcium-Activated Potassium ChannelsKCNN4 protein, humanNOD2 protein, humanNod2 Signaling Adaptor ProteinRNA, Messenger

Identifiers

PMID23160753
OpenAlexW2088764647

What OpenQuestion holds

Textmetadata
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.