Innate immunity during bacterial infection
Bacterial pathogens like S. aureus have evolved an arsenal of virulence strategies to subvert the immune response. S. aureus infections frequently require antibiotics to resolve, but as viable antibiotic treatments for S. aureus narrow, understanding the interactions at the host-pathogen interface is critical to developing future therapeutics. We seek to understand how neutrophils detect disruptions elicited by bacterial pathogens and shape their inflammatory processes like neutrophil extracellular trap (NET) release to suit the constants of the environment.

Immunometabolism regulating pathogen clearance There exists a delicate balance between metabolic and inflammatory pathways allowing for pathogen clearance and limiting host tissue damage; however perturbations in this equilibrium promote disease. Comorbidities like diabetes, obesity, and autoimmune disease associate with massive shifts in metabolic homeostasis coinciding with an increased risk for bacterial infection. We seek to decipher how these changes to metabolism affect myelopoiesis and downstream neutrophil effector function in dysregulating inflammation during infection.