Mechanisms of Innate Immune Regulation of Dermonecrosis during Staphylococcus aureus skin infections

Abstract

S. aureus is the dominant cause of skin and soft tissue infections (SSTIs) in humans. The importance of S. aureus as the primary cause of skin infections has increased exponentially over the last few decades since the emergence of resistance to β-lactam antibiotics. Furthermore, the rise of methicillin-resistant S. aureus (MRSA) strains has led to hospitals stays, increased financial burden and increased mortality. A significant proportion of MRSA infections have been attributed to community-acquired strains (CA-MRSA), specifically the USA300 isolates, which can cause deadly disease in otherwise healthy individuals. Due to the increase in antibiotic resistance and the lack of an effective vaccine against S. aureus, there is a limit in current treatment options available for infected patients and a need for better therapeutics that limit resistance while fighting infection. In order to design better therapeutics to combat S. aureus, it is imperative to understand the host innate immune factors that are protective against S. aureus. Our work focuses on the role of the scavenger receptor CD36 in regulation of the host inflammatory response during S. aureus skin infection, sex bias in susceptibility to infection with S. aureus, and the role of estrogen in host defense during infection. This work is especially important for patient populations which show increased susceptibility to infection due to dysfunctional innate immune mechanisms