Cefoperazone prevents the inactivation of alpha(1)-antitrypsin by activated neutrophils

At sites of neutrophilic inflammation, tissue injury by neutrophil elastase is favored by phagocyte-induced hypochlorous acid dependent inactivation o f the natural elastase inhibitor alpha(1)-antitrypsin. In the present study , cefoperazone prevented alpha(1)-antitrypsin inactivation by neutrophils a nd reduced the recovery of hypochlorous acid from these cells. Moreover, th e antibiotic reduced the free elastase activity in a neutrophil suspension supplemented with alpha(1)-antitrypsin without affecting the cells' ability to release elastase. These data suggest that the drug inactivates hypochlo rous acid before its reaction with alpha(1)-antitrypsin, thereby permitting the antiprotease-mediated blockade of released elastase. In conclusion, ce foperazone appears to have the potential for limiting elastase-antielastase imbalances, attenuating the related tissue injury at sites of inflammation .