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At sites of neutrophilic inflammation, tissue injury by neutrophil elastase is favored by phagocyte-induced hypochlorous acid-dependent inactivation of the natural elastase inhibitor α1 -antitrypsin. In the present study, cefoperazone prevented α1 -antitrypsin inactivation by neutrophils and reduced the recovery of hypochlorous acid from these cells. Moreover, the antibiotic reduced the free elastase activity in a neutrophil suspension supplemented with α1 -antitrypsin without affecting the cells’ ability to release elastase. These data suggest that the drug inactivates hypochlorous acid before its reaction with α1 -antitrypsin, thereby permitting the antiprotease-mediated blockade of released elastase. In conclusion, cefoperazone appears to have the potential for limiting elastase-antielastase imbalances, attenuating the related tissue injury at sites of inflammation.

Cefoperazone Prevents the Inactivation of α 1 -Antitrypsin by Activated Neutrophils