In‐vitro Activity of Amikacin on the Respiratory Burst Response in Human Polymorphonuclear Neutrophils

Abstract

Polymorphonuclear neutrophils (PMNS) are a major component of the defence mechanism against bacterial infections with the respiratory burst after subsequent activation of the oxidative metabolism and the generation of reactive oxygen species. In this study, the influence of an aminoglycoside antibiotic, amikacin, on the oxidative burst responsiveness of neutrophils, represented by the release of hydrogen peroxide (H2O2), was investigated in-vitro in time-dependent cellular experiments and in a cell-free system. In the cellular model with 2 h incubation time, amikacin (10 mg L−1 −1 g L−1) enhanced the H2O2 release by stimulated PMNs. For higher concentrations (1–5 g L−1) which are not used therapeutically, the H2O2 production was decreased. The pro-oxidant activity of amikacin may be due to a cellular mechanism through the oxidative metabolism of neutrophils as demonstrated in the cell washing experiment. The antioxidant activity observed for the higher concentrations only may be a result of a scavenging effect, as demonstrated in the cell-free system. Thus, by increasing their hydrogen peroxide production, amikacin at therapeutic concentrations enhanced the bactericidal functions of neutrophils.