Neutrophil apoptosis is modulated by endothelial transmigration and adhesion molecule engagement

摘要: Termination of a neutrophil-mediated inflammatory response occurs through the activation endogenous cell death program, apoptosis. Neutrophil apoptosis is constitutive process that can be accelerated or delayed by signals from microenvironment. Since cellular localization at site an challenge critical first step in neutrophil response, we investigated effects transendothelial transmigration on kinetic expression Neutrophils isolated rat lung following with LPS demonstrated significant delay spontaneous This was consequence transmigration, since comparable seen when TNF-alpha, potent inducer vitro, used as stimulus. Human neutrophils delays vitro migration across endothelial monolayer to FMLP. Delayed only occurred cells had been primed LPS, stimulus shown up-regulate beta2 integrins and down-regulate L-selectin. Finally, crosslinking CD11a CD11b, but not CD18, mAbs F(ab')2 fragments produced apoptosis, whereas L-selectin mAb its natural ligand, sulfatides, apoptotic process. Cells which inhibited persistent functional respiratory burst activity. These observations establish role for regulation suggest adhesion molecules serve modulatory programmed death.