Delta-toxin from Staphylococcus aureus as a costimulator of human neutrophil oxidative burst.

Abstract

Delta-toxin from Staphylococcus aureus is responsible for various pathophysiologic effects. By studying different cell types in binding of delta-toxin in low, noncytotoxic concentrations, a specific binding of fluorescein-labeled delta-toxin to neutrophils and monocytes was found. Studying direct effects of delta-toxin on neutrophils, a dose-dependent up-regulation of complement receptor 3 expression was found. Oxygen radical production, as determined by Luminol-enhanced chemiluminescence, was not directly induced by delta-toxin, and this toxin was also unable to prime neutrophils for an enhanced response to FMLP or complement-opsonized zymosan. However, the priming response induced by lipopolysaccharide or tumor necrosis factor-alpha (TNF-alpha) was significantly further enhanced in the presence of delta-toxin. Furthermore, as a direct effect on human monocytes, delta-toxin induced TNF-alpha production. These data provide evidence that delta-toxin has direct and indirect effects on the activity of neutrophils and monocytes with regard to its proinflammatory capacity.