The diabetic environment perpetuates Staphylococcus aureus infection

The hypothesis of this study is that hyperglycemia supports S. aureus infection. To address this question, the PI established a diabetic mouse model of subcutaneous skin infection and will investigate whether diabetes affects (i) clearance, (ii) pathogenesis, and (iii) immune response to S. aureus skin infection. He has shown that diabetic mice have increased dermal necrosis and delayed resolution of infection in response to S. aureus infection. This work establishes a model to investigate S. aureus skin infection in the context of diabetes. Using this model, the PI will determine the effects of glucose on immune cell function and test the hypothesis that hyperglycemia inhibits the phagocytic and killing function of macrophages and neutrophils as well as their ability to properly invoke an inflammatory response. By using cells exposed to varying levels of glucose as well as cells isolated from control and diabetic mice he will investigate whether phagocytes have diminished bacterial killing capacity and reduced ability to induce inflammatory cytokines.