[Quinolones and phagocytosis]

Abstract

Fluoroquinolones as pefloxacin (PEF), ciprofloxacin (CIP), ofloxacin (OFL), norfloxacin (NOR) and enoxacin (ENO), are able to interfere with phagocyte-bacteria interaction. Active forms of PEF, CIP and OFL are concentrated in macrophages (MA) and polymorphonuclear leukocytes (PMN). These molecules appear to be free in MA cytoplasm and their release is rapid after withdrawal of extracellular antibiotic. Pretreatment of different species of bacteria (Enterobacteriaceae, S. aureus) with sub-CMIs of CIP and PEF, leads to morphologic modifications of bacteria and increases their engulfment by PMNs. Pretreatment of PMNs with therapeutic concentrations of PEF, NOR and ENO, but not CIP, increases phagocytic capacity and/or chemiluminescence. S. aureus pretreatment with sub-CMIs of CIP enhances intracellular killing. Adding of PEF after L. pneumophila phagocytosis by MA, involves a significant intracellular killing even after withdrawal of the extracellular drug. These different properties could explain good therapeutic results in severe infection treatment when the antibacterial activity of an antibiotic is not really sufficient to cure the infectious disease.