V体育2025版 - Toll-like receptor 2 controls mucosal inflammation by regulating epithelial barrier function
- PMID: 17408640
- DOI: V体育官网入口 - 10.1053/j.gastro.2007.02.056
Toll-like receptor 2 controls mucosal inflammation by regulating epithelial barrier function (V体育安卓版)
Abstract
Background & aims: Toll-like receptors (TLRs) represent a class of transmembrane pattern recognition receptors essential for microbial recognition and control of innate immune responses. Commensal bacteria play an important role in maintaining tolerance and active stability of the intestinal epithelial barrier by suppressing intestinal inflammation, yet the mechanisms of action are unknown. The aim of this study was to determine the functional relevance of TLR2 to control tight junction (TJ)-associated intestinal epithelial barrier integrity to balance mucosal homeostasis against inflammatory stress-induced damage. VSports手机版.
Methods: TLR2 ligand (synthetic Pam(3)Cys-SK4 [PCSK])-induced activation of signaling cascades and TJ-associated distribution was assessed by using Western blotting and confocal microscopy combined with functional transfection and inhibitor studies in model intestinal epithelial cell (IEC) lines (IEC-6, Caco-2) or primary IEC cultured short-term ex vivo V体育安卓版. DSS colitis was induced by standard protocol in wild-type, TLR2-/-, and MyD88-/- mice. Spontaneous apoptosis was assessed by terminal deoxinucleotidyl-transferase-mediated dUTP-biotin nick end-labeling. .
Results: Data from in vitro and ex vivo models of intestinal epithelial cells revealed that TLR2 stimulation effectively preserves TJ-associated barrier assembly against stress-induced damage through promotion of PI3K/Akt-mediated cell survival via MyD88 V体育ios版. Furthermore, in vivo studies underscored that TLR2-mediated TJ regulation critically determines susceptibility to intestinal injury and inflammation. Inflammatory stress in mice deficient of TLR2 or MyD88 induced early TJ-associated disruption interrelated with anti-apoptotic failure of the intestinal epithelial barrier. Oral treatment of colitis with the TLR2 ligand PCSK significantly suppressed mucosal inflammation and apoptosis by efficiently restoring TJ-associated integrity of the intestinal epithelium in vivo. .
Conclusion: TLR2 may provide a target to pharmacologically modulate mucosal injury and intestinal inflammation VSports最新版本. .
Publication types
V体育ios版 - MeSH terms
- "V体育ios版" Actions
- "VSports最新版本" Actions
- Actions (VSports手机版)
- VSports app下载 - Actions
- V体育平台登录 - Actions
- "V体育官网" Actions
- Actions (V体育2025版)
- "VSports最新版本" Actions
- Actions (V体育ios版)
- Actions (VSports在线直播)
- V体育ios版 - Actions
- "V体育2025版" Actions
Substances
- "VSports在线直播" Actions
- V体育官网入口 - Actions
- "VSports app下载" Actions
- Actions (VSports手机版)
Grants and funding
VSports手机版 - LinkOut - more resources
VSports - Full Text Sources
Other Literature Sources
V体育2025版 - Molecular Biology Databases
Miscellaneous