Antibiotics play an important role in helping the host fight infection; however, the direct cellular effect of antibiotics on polymorphonuclear cells remains undefined. Adherence, chemotaxis, phagocytosis, and superoxide anion production are important steps in the cascade of events initiated by the polymorphonucleocyte in bacterial killing. Previous studies have shown inhibition as well as stimulation of neutrophil antibacterial therapy by antibiotics. Peritoneal and blood polymorphonuclear neutrophils (PMN) respond differently to peritonitis and to external agents. The purpose of this study was to investigate the effects of in vivo clindamycin and netilmicin on infected rabbit peritoneal and blood polymorphonuclear adhesiveness, phagocytosis, chemotaxis, and superoxide anion production. Peritoneal and blood PMNs were obtained from rabbits which had undergone appendiceal devascularization 18 hr earlier: antibiotics were administered intramuscularly 1 hr prior to appendectomy and every 8 hr postoperatively for 5 days; these PMNs were compared to infected rabbits which did not receive antibiotics. Clindamycin and netilmicin in vivo cause significant inhibition of phagocytosis, peritoneal adhesiveness, and, when used in combination, blood adhesiveness and peritoneal superoxide anion production. No effects were seen on chemotaxis. Based on this data we conclude that antibiotics, while vitally important in fighting infections, may in and of themselves be agents of immunosuppression at the cellular level.
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