Postischemic vascular permeability requires both TLR-2 and TLR-4, but only TLR-2 mediates the transendothelial migration of leukocytes.

摘要: Ischemia-reperfusion (I/R) activates innate immunity involving Toll-like receptor (TLR) 2 and TLR-4 signaling. Leukocyte migration vascular permeability contribute to postischemic tissue damage. We hypothesized that TLR-2 directly mediate leukocyte during I/R. used in vivo microscopy on murine cremaster muscle quantify adhesion as well transendothelial interstitial sham-operated wild-type mice wild-type, TLR-2(-/-), TLR-4-mutant 30 120 min after Alterations fluorescein isothiocyanate-dextran leakage across cremasteric venules were determined a measure of endothelial permeability. I/R-induced TLR-2(-/-) was comparable mice. The number transmigrated leukocytes increased upon I/R compared with the group. In contrast, transmigration significantly attenuated but not Motility polarization interstitially migrating did differ from Postischemic lower both than conclude signaling enhance has additional effects at wall.