Evidence map›Paper›PMID 26451337›Full record

ArticleTissue barriers

Commensal bacterial internalization by epithelial cells: An alternative portal for gut leakiness.

Linda Chia-Hui Yu

Open access · bronzeAbstract read
In one paragraph

Article in Tissue barriers. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

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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 2 countries.

Linda Chia-Hui YuGraduate Institute of Physiology; National Taiwan University ; Taipei, Taiwan, Republic of China.
Czech Academy of Sciences, Institute of Physiology · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Co-existing paracellular and transcellular barrier defect in intestinal epithelium was documented in inflammatory bowel disease, celiac disease, and intestinal obstruction. Mechanisms regarding tight junction disruption have been extensively studied; however, limited progress has been made in research on bacterial transcytosis. Densely packed brush border (BB), with cholesterol-based lipid rafts in the intermicrovillous membrane invagination, serves as an ultrastructural barrier to prevent direct contact of luminal microbes with the cellular soma. Evidence in in vitro epithelial cell cultures and in vivo animal models of bowel obstruction and antibiotic-resistant bacterial infection had indicated that nonpathogenic, noninvasive enteric bacteria may hijack the lipid raft-mediated endocytic pathways. Our studies have shown that low dose interferon-gamma (IFNγ) causes long myosin light chain kinase (MLCK)-dependent terminal web (TW) contraction and BB fanning, allowing bacteria to pass through the consequently widened intermicrovillous cleft to be endocytosed via caveolin-associated lipid rafts. Activation of intracellular innate immune receptors by bacteria-containing endosomes may further induce inflammatory and oxidative stress, leading to secondary tight junction damage. The finding of bacterial internalization preceding tight junction damage suggests that abnormal bacterial uptake by epithelial cells may contribute to the initiation or relapse of chronic intestinal inflammation.

Indexed as

bacterial endocytosisbrush borderinnate immune receptorsMLCKproinflammatory cytokines

Identifiers

PMID26451337
PMCPMC4574896
OpenAlexW1589335048

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.