Clindamycin at Subinhibitory Concentrations Enhances Antibody- and Complement-Dependent Phagocytosis by Human Polymorphonuclear Leukocytes of <i>Staphylococcus aureus</i>

Abstract

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.

Effect of Linezolid on the Phagocytic Functions of Human Polymorphonuclear Leukocytes

“…Some antimicrobials can penetrate and remain active within the phagocytes [3,4]. The effect of other agents on phagocytosis may however be secondary to the exposure of bacteria to low concentrations of antimicrobials [5,6].…”

Effect of Ampicillin/Sulbactam on Human Polymorphonuclear Leukocyte Function

“…The process of phagocytosis, the most im portant mechanism against different bac teria, can be modulated by some antimi crobial agents [1,2). Some antimicrobials can penetrate and remain active within the phagocytes [3,4], The effect of other agents on phagocytosis may however be secondary to the exposure of bacteria to low concentrations of antimicrobials [5,6], In recent years potent |l-lactamasc in hibitors such as clavulanic acid and sulbac tam have become available for halting the action of common (3-lactamase. There is not much information, however, on the in teraction of p-lactamase inhibitors on host defense mechanisms.…”

Pretreatment of Mice with Clindamycin Improves Survival of Endotoxic Shock by Modulating the Release of Inflammatory Cytokines

“…Furthermore, the administration of fosfomycin (FOF) led to a reduction in serum TNF alpha (TNF-␣) and IL-1␤ concentrations in LPS-stimulated mice (9). Clindamycin (CLI), which is effective against gram-positive and anaerobic bacteria, has been demonstrated to induce neutrophil phagocytosis in the host at subMIC levels (18,19). We have previously reported that CLI significantly suppressed TNF-␣ release from purified LPS-stimulated human acute monocytic leukemic cell line (THP-1) in vitro (7).…”