Neutrophil-mediated solubilization of the subendothelial matrix: oxidative and nonoxidative mechanisms of proteolysis used by normal and chronic granulomatous disease phagocytes.

摘要: Both normal and chronic granulomatous disease (CGD) neutrophils were able to degrade the subendothelial matrix secreted by human endothelial cells via an elastase-dependent process. In absence of plasma antiproteinase, alpha-1-proteinase inhibitor (alpha-1-PI), protect their released elastase from inactivation using chlorinated oxidants hypochlorous acid endogenous N-chloroamines suppress antiproteinase's activity. contrast, CGD unable generate either class oxidant or inactivate porcine pancreatic inhibitory capacity alpha-1-PI unless supplemented with exogenous hydrogen peroxide. Despite reliance on alpha-1-PI, triggered in presence agents that block generation these reactive species continued at a suppressed but significant rate 50-fold excess antiproteinase. The solubilization was not due incomplete inhibition because also alpha-1-PI. If stimulated source H2O2 proteolytic potential identical observed neutrophils. We conclude can enhance ability oxidatively protecting both possess non-oxidatively linked mechanisms for sequestering mediate effects native