Staphylococcus aureus β-Hemolysin Up-Regulates the Expression of IFN-γ by Human CD56bright NK Cells

IFN-gamma is produced upon stimulation with S. aureus and may play a detrimental role during infection. However, whether hemolysins play a role in the mechanism of IFN-gamma production has not been fully characterized. In this study, we demonstrated that Hlb, one of the major hemolysins of S. aureus, upregulated IFN-gamma production by CD56(bright) NK cells from human peripheral blood mononuclear cells (PBMCs). Further investigation showed that Hlb increased calcium influx and induced phosphorylation of ERK1/2. Either blocking calcium or specifically inhibiting phosphorylation of ERK1/2 decreased the production of IFN-gamma induced by Hlb. Moreover, we found that this process was dependent on the sphingomyelinase activity of Hlb. Our findings revealed a novel mechanism of IFN-gamma production in NK cells induced by Hlb, which may be involved in the pathogenesis of S. aureus.

Automated summary

The study demonstrates that the hemolysin Hlb of S. aureus can upregulate IFN-gamma production in target cells by increasing calcium influx and inducing phosphorylation of ERK1/2. This process is dependent on the sphingomyelinase activity of Hlb.