ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Mechanism of IL-1β modulation of intestinal epithelial barrier involves p38 kinase and activating transcription factor-2 activation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
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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.
The trial behind it
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Who cites it
78 citing papers in PubMed, 140 citations in OpenAlex.
- Recurrent Severe Subclinical Mastitis and the Risk of HIV Transmission Through Breastfeeding.Frontiers in immunology · 2022Trial
- A Double-Blind, Randomized Placebo-Controlled Trial of ProbioticNutrients · 2020Trial
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Oxidative Stress-Gut Microbiome Crosstalk: Intestinal Redox Imbalance and Probiotics Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2026Review
- Conformable Device for Independent Measurements of Mucosal and Vascular Barriers in a Complex In Vitro Intestinal Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Effects of supplementing diet withFrontiers in microbiology · 2026Article
- Towards a basis for vascular versus intestinal phenotype differences; East Meets West in Behcet's disease.Frontiers in immunology · 2026Review
- Microbial threads in the tapestry of rheumatoid arthritis.The Journal of clinical investigation · 2025Review
- The regulatory effects of epigallocatechin gallate on growth performance, systemic antioxidant status, immune response, and gut microbiota structure in geese.Poultry science · 2025Article
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- Enteric glial NLRP3 inflammasome contributes to gut mucosal barrier alterations in a mouse model of diet-induced obesity.Acta physiologica (Oxford, England) · 2025Article
- Tight junction regulation, intestinal permeability, and mucosal immunity in gastrointestinal health and disease.Current opinion in gastroenterology · 2025Review
- Neisseria gonorrhoeae induces local secretion of IL-10 at the human cervix to promote colonization.The Journal of clinical investigation · 2024Article
- Modulation of Serotonin-Related Genes by Extracellular Vesicles of the ProbioticInternational journal of molecular sciences · 2024Article
- Molecular mechanism of MLCK1 inducing 5-Fu resistance in colorectal cancer cells through activation of TNFR2/NF-κB pathway.Discover oncology · 2024Article
- A Comparative Study on the Effects of Mesenchymal Stem Cells and Their Conditioned Medium on Caco-2 Cells as an In Vitro Model for Inflammatory Bowel Disease.International journal of cell biology · 2024Article
- Paracellular permeability and tight junction regulation in gut health and disease.Nature reviews. Gastroenterology & hepatology · 2023Review
- A Comparative Study on the Effects of Different Sources of Carboxymethyl Poria Polysaccharides on the Repair of DSS-Induced Colitis in Mice.International journal of molecular sciences · 2023Article
- Long-Term Use of Proton Pump Inhibitors Disrupts Intestinal Tight Junction Barrier and Exaggerates Experimental Colitis.Journal of Crohn's & colitis · 2023Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The defective intestinal epithelial tight junction (TJ) barrier has been postulated to be an important pathogenic factor contributing to intestinal inflammation. It has been shown that the proinflammatory cytokine IL-1β causes an increase in intestinal permeability; however, the signaling pathways and the molecular mechanisms involved remain unclear. The major purpose of this study was to investigate the role of the p38 kinase pathway and the molecular processes involved. In these studies, the in vitro intestinal epithelial model system (Caco-2 monolayers) was used to delineate the cellular and molecular mechanisms, and a complementary in vivo mouse model system (intestinal perfusion) was used to assess the in vivo relevance of the in vitro findings. Our data indicated that the IL-1β increase in Caco-2 TJ permeability correlated with an activation of p38 kinase. The activation of p38 kinase caused phosphorylation and activation of p38 kinase substrate, activating transcription factor (ATF)-2. The activated ATF-2 translocated to the nucleus where it attached to its binding motif on the myosin L chain kinase (MLCK) promoter region, leading to the activation of MLCK promoter activity and gene transcription. Small interfering RNA induced silencing of ATF-2, or mutation of the ATF-2 binding motif prevented the activation of MLCK promoter and MLCK mRNA transcription. Additionally, in vivo intestinal perfusion studies also indicated that the IL-1β increase in mouse intestinal permeability required p38 kinase-dependent activation of ATF-2. In conclusion, these studies show that the IL-1β-induced increase in intestinal TJ permeability in vitro and in vivo was regulated by p38 kinase activation of ATF-2 and by ATF-2 regulation of MLCK gene activity.
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Registered trials
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.