Clindamycin at subinhibitory concentrations enhances antibody- and complement-dependent phagocytosis by human polymorphonuclear leukocytes of Staphylococcus aureus.
The influence of subinhibitory concentrations of clindamycin on opsonization and phagocytosis of Staphylococcus aureus was studied. S. aureus was grown overnight in the presence or absence of one half or one quarter of the minimal inhibitory concentration (MIC) of clindamycin. Radioactively labeled S. aureus was opsonized for various periods of time in different concentrations of normal serum, heated antiserum and serum of patients with agammaglobulinaemia or C3 deficiency. Complement- as well as antibody-dependent phagocytosis of the antibiotic treated S. aureus was significantly enhanced, compared to phagocytosis of the untreated control. Killing experiments showed that clindamycin-treated S. aureus was also better killed by the granulocytes than untreated S. aureus. The mechanism of action is likely to be an increased susceptibility of clindamycin-treated bacteria to antibody- and complement-dependent phagocytosis.
D000361:Agammaglobulinemia / Q000276:immunology; D001770:Blood Bactericidal Activity / Q000187:drug effects; D002981:Clindamycin / Q000494:pharmacology*; D003176:Complement C3 / Q000172:deficiency / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D007700:Kinetics; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology; D009895:Opsonin Proteins / Q000502:physiology; D010587:Phagocytosis / Q000187:drug effects*; D013211:Staphylococcus aureus / Q000276:immunology*
D003176:Complement C3; D009895:Opsonin Proteins; D002981:Clindamycin