Effect of Staphylococcus aureus enterotoxin F on human neutrophil oxidative metabolism

Epidemiologic and animal challenge studies have suggested that SEF may play a critical role in toxic-shock syndrome [1]. However, the pathogenic mechanism of SEF activity is not known. One means by which this toxin could elicit the widespread organ dysfunction observed in toxic-shock syndrome would be by directly promoting PMN production of toxic oxygen species and the resultant secondary endothelial cell damage [2]. To evaluate this possibility, we assayed the effect of SEF on PMN oxidative metabolism. SEF at 0.01-100 ng/ml did not stimulate O2- release or O2 consumption by inactive PMNs. Similarly, incubation of PMNs with 10 ng of SEF/ml for 1 hr neither potentiated nor inhibited cellular O2 consumption stimulated by optimal (10 mg/ml) or suboptimal (0.1 mg/ml) concentrations of opsonized zymosan. Finally, SEF had no effect on O2- release by PMNs stimulated by PMA. PMN viability, as assessed by trypan blue exclusion, was unaffected by SEF. This study did not address the possibility that SEF might indirectly activate PMN oxidative metabolism by promoting leukocytic pyrogen production by monocytes and macrophages [3]. SEF neither directly activated PMN oxidative activity nor potentiated the cellular oxidative response to particulate or soluble stimuli. Consequently, direct stimulation of PMN-derived, O2- mediated damage to endothelial cells is not a tenable hypothesis to explain the mechanism of SEF toxicity.