Our research examines how pathogens interact with the immune system. A major interest is Streptococcus pyogenes (group A Strep; GAS), because:

...it is a familiar and highly prevalent pathogen; yearly infection rates approach one billion (mostly in children as strep throat)

...it is a top 10 pathogen in morbidity and mortality (through diseases like sepsis, toxic shock syndrome, necrotizing fasciitis, glomerulonephritis, rheumatic fever, and rheumatic heart disease)

...relative to other major pathogens, we have little insight on GAS pathogenesis

...we have no vaccine 

...and, antibiotic prescription for presumptive GAS is a leading contributor to the spread of antibiotic resistance

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A hallmark of GAS infections is their strongly inflammatory nature. We recently found this is due in part to a GAS protease activating the inflammatory cytokine IL-1β via an alternative pathway. Our current research expands from these discoveries to ask:

How do GAS, inflammation, and the microbiome interact during infection?

Which GAS virulence factors contribute to the development of different diseases?

What is the significance of ‘alternative’ IL-1β activation in other infections and inflammatory diseases?

How can opportunistic pathogens take advantage of pharmaceutical modulation of immunity? How can we use repurposed drugs to treat infection?