Probiotics inhibit nuclear factor-κB and induce heat shock proteins in colonic epithelial cells through proteasome inhibition

摘要: Background & Aims: The extent and severity of mucosal injury in inflammatory bowel diseases are determined by the disequilibrium between 2 opposing processes: reparative cytoprotective mechanisms vs. inflammation-induced injury. Probiotics may provide clinical benefit ameliorating colitis; however, their action remain largely unknown. Our objective was to investigate microbial-epithelial interactions that could explain beneficial therapeutic effects probiotics. Methods: effect VSL#3-conditioned media on nuclear factor-κB pathway young adult mouse colonic epithelial cells assessed using monocyte chemoattractant protein-1 enzyme-linked immunosorbent assays; IκBα, IκBβ, p105 immunoblot analysis; luciferase reporter gene proteasome assays. Effects heat shock proteins were electrophoretic mobility shift assay for 25 72 cells. Cytoprotection against oxidant chromium 51 release filamentous globular actin Results: VSL#3 produces soluble factors inhibit chymotrypsin-like activity gut Proteasome inhibition is an early event begins almost immediately after exposure probiotic-conditioned media. In addition, these bacteria proinflammatory through a mechanism different from type III secretory described other nonpathogenic enteric flora. They also induce expression intestinal Conclusions: resulting increased account anti-inflammatory reported probiotics be novel interaction. These seem mediated common unifying inhibition.