ArticleThe American journal of pathology2019
Lipopolysaccharide-Induced Increase in Intestinal Permeability Is Mediated by TAK-1 Activation of IKK and MLCK/MYLK Gene.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 93 citations in OpenAlex.
- Acute liver injury is triggered by dysbiosis and microbial translocation involving gut-liver axis.Gut microbes · 2026Article
- Endotoxins and Biological Implications-Review.Public health challenges · 2026Review
- Ethanol, acetaldehyde, lipopolysaccharide, and neutrophil extracellular traps: four-pronged attack on gut epithelial barrier in alcohol use disorder.Anatomical record (Hoboken, N.J. : 2007) · 2026Review
- Microbiota-Inflammation Crosstalk in Myeloproliferative Neoplasms: MPN-Specific Human Data, Mechanistic Plausibility and Translational Priorities.Biomedicines · 2026Review
- Article
- Beyond the Ribosome: The Expanding Role of the Nucleolus in Neurodegenerative Pathways.Molecular neurobiology · 2026Review
- Exploring Endotoxemia in Age-Related Macular Degeneration, Glaucoma, and Diabetic Retinopathy.Investigative ophthalmology & visual science · 2026Review
- Multi-omics reveals soybean meal-induced gut microbiota alterations and metabolic disturbances in largemouth bass (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Dietary Taurine Enhances Intestinal Digestion, Absorption, and Villus Morphology in Mice.Animals : an open access journal from MDPI · 2026Article
- Effects of specialized proresolving mediators on gut epithelial barrier in early life.The Journal of pharmacology and experimental therapeutics · 2026Article
- The Barrier-Microbiota-Inflammation Axis in Colorectal Cancer: Mechanisms and Emerging Diagnostic & Therapeutic Strategies.Cancers · 2026Review
- Quercetin ameliorates HIV-1 gp120 protein-induced intestinal barrier dysfunction by inhibiting the activation of the ERK1/2 signaling pathway in a Caco-2 cell model.AIDS research and therapy · 2026Article
- Transfer factor alleviates bovine mastitis and protects mammary epithelial barrier via the TAK1/NF-κB/MLCK signaling axis.Journal of animal science · 2026Article
- From dysbiosis to dysfunction: specific gut microbes and metabolites in the pathogenesis of Parkinson's disease.Sustainable microbiology · 2026Review
- Fermented cotton stalks preserve colonic epithelial integrity in Hu sheep via the microbiota-metabolite-NF-κB/MLCK axis and mitigate the adverse effects of direct feeding.Frontiers in nutrition · 2026Article
- Gut microbiota and the tryptophan-kynurenine pathway in anxiety: new insights and treatment strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Filamentous bacteriophage M13 induces proinflammatory responses in intestinal epithelial cells.Infection and immunity · 2025Article
- Macronutrients as Regulators of Intestinal Epithelial Permeability: Where Do We Stand?Comprehensive reviews in food science and food safety · 2025Review
- Glucagon-Like Peptide-1 Is Prognostic of Mortality in Acute Respiratory Failure.Critical care explorations · 2025Article
- Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Lipopolysaccharides (LPSs) are a major component of Gram-negative bacterial cell wall and play an important role in promoting intestinal inflammatory responses. Recent studies have shown that physiologically relevant concentrations of LPS (0 to 2000 pg/mL) cause an increase in intestinal epithelial tight junction (TJ) permeability without causing cell death. However, the intracellular pathways and the mechanisms that mediate LPS-induced increase in intestinal TJ permeability remain unclear. The aim was to delineate the intracellular pathways that mediate the LPS-induced increase in intestinal permeability using in vitro and in vivo intestinal epithelial models. LPS-induced increase in intestinal epithelial TJ permeability was preceded by an activation of transforming growth factor-β-activating kinase-1 (TAK-1) and canonical NF-κB (p50/p65) pathways. The siRNA silencing of TAK-1 inhibited the activation of NF-κB p50/p65. The siRNA silencing of TAK-1 and p65/p50 subunit inhibited the LPS-induced increase in intestinal TJ permeability and the increase in myosin light chain kinase (MLCK) expression, confirming the regulatory role of TAK-1 and NF-κB p65/p50 in up-regulating MLCK expression and the subsequent increase in TJ permeability. The data also showed that toll-like receptor (TLR)-4/myeloid differentiation primary response (MyD)88 pathway was crucial upstream regulator of TAK-1 and NF-κB p50/p65 activation. In conclusion, activation of TAK-1 by the TLR-4/MyD88 signal transduction pathway and MLCK by NF-κB p65/p50 regulates the LPS-induced increase in intestinal epithelial TJ permeability.
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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.