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Preliminary studies suggest that Lipopolysaccharides (LPS)(brain://xt1-tHoWL0OtAZuS_LDW9Q/LipopolysaccharidesLps), LPS-binding protein, and zonulin may be involved in the pathophysiology of increased intestinal permeability
Interleukin-1 (IL-1) beta (IL-1F2)-induced increase in intestinal TJ permeability is an important contributing factor of intestinal inflammation. IL-1 b causes a rapid and marked leaky gut. This occurs, on the one hand, through activation of the canonical NFKB signaling pathway with subsequent activation of the MLCK gene and, on the other hand, through the post-transcriptional degradation of occludin mRNA
In addition to MLCK gene activation leading to gut barrier opening, IL-1beta increases intestinal TJ permeability through post-transcriptional degradation of occludin mRNA. IL-1b selectively decreases occludin levels in mouse Caco-2 monolayers and intestinal epithelial cells. IL-1 b causes a rapid increase in miRNAs that bind to occludin mRNA (miR 200c-3p binding to the occludin 3'-UTR)
An increase in microRNA-200c-3p (miRNA 200c-3p) expression in IECs causes intestinal TJ permeability in Caco-2 cells and mice. Antagomirs that inhibit or silence microRNA-200c-3p (miRNA 200c-3p) inhibit the IL-1 b -induced decrease in occludin expression and increased intestinal epithelial TJ permeability
DSS causes a marked increase in IL1 b-dependent microRNA-200c-3p (miRNA 200c-3p) expression in gut tissue with a decrease in occludin expression and an increase in colonic permeability. AntogomiR-200c inhibited this effect
see also:
Barrier Permeability / Intestinal Permeability & Tight-Junction Molecules / Tight Junction Proteins