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Staphylococcus aureus  ( S. aureus ) causes a range of diseases ranging from superficial skin and soft-tissue infections to invasive and life-threatening conditions ( Klevens et al., 2007 ;  Kobayashi et al., 2015 ).  S. aureus  utilizes the Sae sensory system to adapt to neutrophil challenge. Although the roles of the SaeR response regulator and its cognate sensor kinase SaeS have been demonstrated to be critical for surviving neutrophil interaction and for causing infection, the roles for the accessory proteins SaeP and SaeQ remain incompletely defined. To characterize the functional role of these proteins during innate immune interaction, we generated isogenic deletion mutants lacking these accessory genes in USA300 (USA300Δ saeP  and USA300Δ saeQ ).  S. aureus  survival was increased following phagocytosis of USA300Δ saeP  compared to USA300 by neutrophils. Additionally, secreted extracellular proteins produced by USA300Δ saeP  cells caused significantly more plasma membrane damage to human neutrophils than extracellular proteins produced by USA300 cells. Deletion of  saeQ  resulted in a similar phenotype, but effects did not reach significance during neutrophil interaction. The enhanced cytotoxicity of USA300Δ saeP  cells toward human neutrophils correlated with an increased expression of bi-component leukocidins known to target these immune cells. A  saeP  and  saeQ  double mutant (USA300Δ saePQ ) showed a significant increase in survival following neutrophil phagocytosis that was comparable to the USA300Δ saeP  single mutant and increased the virulence of USA300 during murine bacteremia. These data provide evidence that SaeP modulates the Sae-mediated response of  S. aureus  against human neutrophils and suggest that  saeP  and  saeQ  together impact pathogenesis  in vivo .

The Accessory Gene saeP of the SaeR/S Two-Component Gene Regulatory System Impacts Staphylococcus aureus Virulence During Neutrophil Interaction