Staphylococcus aureus, Antibiotic Resistance, and the Interaction with Human Neutrophils

Staphylococcus aureus is among the leading causes of bacterial infections worldwide. The high burden of S. aureus among human and animal hosts, which includes asymptomatic carriage and infection, is coupled with a notorious ability of the microbe to become resistant to antibiotics. Notably, S. aureus has the ability to produce molecules that promote evasion of host defense, including the ability to avoid killing by neutrophils. Significant progress has been made to better understand S. aureus-host interactions. These discoveries include elucidation of the role played by numerous S. aureus virulence molecules during infection. Based on putative functions, a number of these virulence molecules, including S. aureus alpha-hemolysin and protein A, have been identified as therapeutic targets. Although it has not been possible to develop a vaccine that can prevent S. aureus infections, monoclonal antibodies specific for S. aureus virulence molecules have the potential to moderate the severity of disease. Therapeutic options for treatment of methicillin-resistant S. aureus (MRSA) are limited, and the microbe typically develops resistance to new antibiotics. New prophylactics and/or therapeutics are needed. Research that promotes an enhanced understanding of S. aureus-host interaction is an important step toward developing new therapeutic approaches directed to moderate disease severity and facilitate treatment of infection. This research effort includes studies that enhance our view of the interaction of S. aureus with human neutrophils. Antioxid. Redox Signal. 34, 452-470.