Mechanism of Bifidobacterium bifidum inhibition of tumor necrosis factor (TNF)-α–induced opening of intestinal tight junction (TJ) barrier (IMAGE)

Elsevier

Mechanism of Bifidobacterium bifidum inhibition of tumor necrosis factor (TNF)-α–induced opening of intestinal tight junction (TJ) barrier

Caption

TNF-α–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 γ (PPAR- γ). The PPAR- γ activation results in inhibition of TNF-α–induced IKK [inhibitor of nuclear factor-κB (IκB) kinase]-α activation, which, in turn, leads to the inhibition of NF-kB activation, MLCK gene activation, and MLCK-induced opening of the TJ barrier. RXR, retinoid X receptor.

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The American Journal of Pathology

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