Abstract
While Staphylococcus aureus accelerates human neutrophil cell death, the underlying host- and pathogen-derived mechanisms remain incompletely defined. Previous studies demonstrated that the S. aureus SaeR/S sensory system is essential for pathogen survival following neutrophil phagocytosis. Herein, we demonstrate that the SaeR/S system promoted accelerated cell death, suppressed phosphorylation of nuclear factor-κB, and reduced interleukin-8 (IL-8) production in human neutrophils. Treatment of neutrophils with recombinant IL-8 significantly reduced bacterial burden and apoptosis. Our findings demonstrate a mechanism by which S. aureus suppresses the early neutrophil-derived IL-8 response to disrupt cell fate and promote disease.