Evidence map›Paper›PMID 18390750›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Mechanism of IL-1beta-induced increase in intestinal epithelial tight junction permeability.

Rana Al-Sadi, Dongmei Ye, Karol Dokladny, Thomas Y Ma

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 2 pooled it
12.0field-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

213 citing papers in PubMed, 2 syntheses or guidelines pooled it, 404 citations in OpenAlex.

  1. Effect ofFrontiers in pharmacology · 2025
    Pooled it
  2. Association between Interleukin-1β Gene -511C>T/+3954C>T Polymorphisms and Aggressive Periodontitis Susceptibility: Evidence from a Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Pooled it
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  17. Probiotics and the intestinal tight junction barrier function.Frontiers in cell and developmental biology · 2025
    Review
  18. Article
  19. Article
  20. Article

153 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

4 authors at 1 institution in 1 country.

Rana Al-SadiDepartment of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.
Dongmei Ye
Karol Dokladny
Thomas Y Ma
University of New Mexico · US

Funding

TNF-alpha Regulation of Intestinal Paracellular TransportR01DK064165 · NIDDK · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI MA, THOMAS Y · 2003 to 2018
$5.2M
NIDDK NIH HHS R01 DK064165NIDDK NIH HHS R01-DK-64165-01
6 · The paper itself

Abstract

The IL-1beta-induced increase in intestinal epithelial tight junction (TJ) permeability has been postulated to be an important mechanism contributing to intestinal inflammation of Crohn's disease and other inflammatory conditions of the gut. The intracellular and molecular mechanisms that mediate the IL-1beta-induced increase in intestinal TJ permeability remain unclear. The purpose of this study was to elucidate the mechanisms that mediate the IL-1beta-induced increase in intestinal TJ permeability. Specifically, the role of myosin L chain kinase (MLCK) was investigated. IL-1beta caused a progressive increase in MLCK protein expression. The time course of IL-1beta-induced increase in MLCK level correlated linearly with increase in Caco-2 TJ permeability. Inhibition of the IL-1beta-induced increase in MLCK protein expression prevented the increase in Caco-2 TJ permeability. Inhibition of the IL-1beta-induced increase in MLCK activity also prevented the increase in Caco-2 TJ permeability. Additionally, knock-down of MLCK protein expression by small interference RNA prevented the IL-1beta-induced increase in Caco-2 TJ permeability. The IL-1beta-induced increase in MLCK protein expression was preceded by an increase in MLCK mRNA expression. The IL-1beta-induced increase in MLCK mRNA transcription and subsequent increase in MLCK protein expression and Caco-2 TJ permeability was mediated by activation of NF-kappaB. In conclusion, our data indicate that the IL-1beta increase in Caco-2 TJ permeability was mediated by an increase in MLCK expression and activity. Our findings also indicate that the IL-1beta-induced increase in MLCK protein expression and Caco-2 TJ permeability was mediated by an NF-kappaB-dependent increase in MLCK gene transcription.

Indexed as

Cell Membrane PermeabilityCaco-2 CellsHumansInterleukin-1betaIntestinal MucosaMyosin-Light-Chain KinaseNF-kappa BRNA, Small InterferingTight JunctionsTranscription, GeneticInterleukin-1betaMyosin-Light-Chain KinaseNF-kappa BRNA, Small Interfering

Identifiers

PMID18390750
PMCPMC3035485
OpenAlexW1902824041

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.