Staphylococcus aureus SaeR/S-regulated Factors Decrease Monocyte-derived TNF-alpha to Reduce Neutrophil Bactericidal Activity


Eli W. Sward, Elizabeth M. Fones, Russel R. Spaan, Kyler B. Pallister, Brandon L. Haller, Fermin E. Guerra, Oliwia W. Zurek, Tyler K. Nygaard, Jovanka M. Voyich


The Journal of Infectious Diseases


The ability of Staphylococcus aureus to evade killing by human neutrophils significantly contributes to disease progression. In this study, we characterize an influential role for the S. aureus SaeR/S-two component gene regulatory system in suppressing monocyte production of TNF-alpha to subsequently influence human neutrophil priming. TNF-alpha production from monocytes was significantly reduced following challenge with wild type S. aureus (USA300) compared to an isogenic saeR/S deletion mutant (USA300?saeR/S). We observed that priming of neutrophils using conditioned medium (CM) from PBMCs stimulated with USA300?saeR/S significantly increased neutrophil bactericidal activity against USA300 relative to unprimed neutrophils and neutrophils primed with USA300 CM. The increased neutrophil bactericidal activity was associated with enhanced ROS production that was significantly influenced by elevated TNF-alpha concentrations. Taken together, our findings identify an immune evasion strategy used by S. aureus to impede neutrophil priming and subsequent bactericidal activity.



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