Effects of clindamycin on human neutrophil functions in vitro

Effects of clindamycin on [Ca²⁺] i in neutrophils, neutrophil chemotaxis, phagocytosis, and reactive oxygen species (ROS) generation were investigated in vitro. ROS generated in a cell-free, xanthine-xanthine oxidase system was also assessed. The species examined were superoxide radical anion (O₂^-), hydrogen peroxide (H₂O₂), and hydroxyl radical (OH·). Clindamycin significantly decreased the levels of O₂^-, H₂O₂, and OH· generated by neutrophils. On the other hand, the drug did not markedly affect [Ca²⁺] i in neutrophils, neutrophil chemotaxis, phagocytosis, and the ROS levels generated in a xanthine-xanthine oxidase system. The present study seems to indicate that clindamycin is not an ROS scavenger but exerts as anti-inflammatory action by inhibiting neutrophil-derived ROS generation at the sites of inflammation.