Proinflammatory Cytokines Disrupt Epithelial Barrier Function by Apoptosis-Independent Mechanisms 1
By Matthias Bruewer, A. Luegering, T. Kucharzik, C. Parkos, J. Madara, A. Hopkins, A. Nusrat. Journal of Immunology, 2003
915 citations recorded by the source corpus.
Subfields: Cell Biology, Immunology, Neurology
View Paper: https://www.semanticscholar.org/paper/ea0b2e5e001bbb0d154502b133d35035b22bf92c
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Citations in the corpus
- A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “IFN-γ increases paracellular permeability and induces endocytosis of tight junction transmembrane proteins [54].”
- Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation. (2010, background): “Alteration in occludin distribution had been reported in ob/ob mice (9), and in vitro on epithelial cells stimulated with proinflammatory cytokines (8), occludin was chosen as a marker of tight junction disruption.”
- Chronic Inflammation and Cytokines in the Tumor Microenvironment (2014, background): “In early IBD pathogenesis, IFN-γ plays an important role in increasing paracellular permeability in T84 epithelial cells by inducing endocytosis of tight-junction (TJ) proteins occludin, JAM-A, and claudin1 [29].”
- Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. (2007, methodology): “The Triton X-100-insoluble residue fraction was passed five times through successive syringes (25, 20, and 18 gauge) in SDS buffer and finally centrifuged at 1,500 g for 5 min at 4°C; this was designated as the insoluble protein fraction (7).”
- Cytokine regulation of tight junctions (2008, background): “MLC phosphorylation increases with combined TNF-α and IFN-γ treatment in Caco-2 epithelial cells [42].”
- Regulation of intestinal epithelial permeability by tight junctions (2012, background): “In intestinal T84 cells, IFN-c induces the cellular internalization of transmembrane TJ proteins (occludin, claudin-1, claudin-4, and JAM-A) from the junctional region, resulting in a decrease in TER and increase in dextran flux [96, 97].”