Staphylococcus aureus inhibits neutrophil-derived IL-8 to promote cell death

While Staphylococcus aureus (S. 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 NF-kB, and reduced 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.

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