A potential pathway may guide new therapies for inflammatory bowel disease and other inflammatory diseases

TNF-?–induced increase in intestinal epithelial TJ permeability is mediated by the activation of NF-kB p50/p65. The activated NF-kB translocates to the nucleus, binds to the cis-kB binding site on the myosin light chain kinase (MLCK) promoter region, and activates the MLCK gene transcription and protein synthesis process. The increase in MLCK protein level and activity [phosphorylated myosin light chain (P-MLC)] results in MLCK-induced opening of the TJ barrier. BB1 treatment activates the toll-like receptor (TLR)-2/TLR-6 signaling pathway, leading to the activation of peroxisome proliferator-activated receptor ? (PPAR- ?). The PPAR- ? activation results in inhibition of TNF-?–induced IKK [inhibitor of Read More