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

Franco Dallegri | Zendy; Patrizia Dapino | Zendy; Nicoletta Arduino | Zendy; Maria Bertolotto | Zendy; Luciano Ottonello | Zendy

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

Author(s) -

Franco Dallegri,

Patrizia Dapino,

Nicoletta Arduino,

Maria Bertolotto,

Luciano Ottonello

Publication year - 1999

Publication title -

antimicrobial agents and chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.07

H-Index - 259

eISSN - 1070-6283

pISSN - 0066-4804

DOI - 10.1128/aac.43.9.2307

Subject(s) - elastase , hypochlorous acid , cefoperazone , neutrophil elastase , inflammation , chemistry , microbiology and biotechnology , pancreatic elastase , alpha (finance) , antibiotics , biochemistry , immunology , enzyme , medicine , biology , antibiotic resistance , imipenem , construct validity , nursing , patient satisfaction

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.

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