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Antimicrobial Agents and Chemotherapy, September 1999, p. 2307-2310, Vol. 43, No. 9
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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

Franco Dallegri,* Patrizia Dapino, Nicoletta Arduino, Maria Bertolotto, and Luciano Ottonello

Department of Internal Medicine, University of Genoa Medical School, Genoa, Italy

Received 11 March 1999/Returned for modification 16 April 1999/Accepted 11 June 1999

At sites of neutrophilic inflammation, tissue injury by neutrophil elastase is favored by phagocyte-induced hypochlorous acid-dependent inactivation of the natural elastase inhibitor alpha 1-antitrypsin. In the present study, cefoperazone prevented alpha 1-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 alpha 1-antitrypsin without affecting the cells' ability to release elastase. These data suggest that the drug inactivates hypochlorous acid before its reaction with alpha 1-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.

* Corresponding author. Mailing address: Semeiotica Medica 2, Dipartimento di Medicina Interna, Viale Benedetto XV n.6, I-16132 Genoa, Italy. Phone: 39 010 3538940. Fax: 39 010 3538638. E-mail: otto{at}csita.unige.it.

Antimicrobial Agents and Chemotherapy, September 1999, p. 2307-2310, Vol. 43, No. 9
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.




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