Christopher N. LaRock, PhD
Microbiology and Immunology
Assistant Professor of Medicine
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Research InterestsPathogens must successfully prevent killing by our immune defenses in order to infect. This is often promoted by virulence factors specifically adapted to intercept key immune factors. We examine this host-pathogen interaction primarily using Streptococcus pyogenes (group A Strep; GAS), a top ten cause of infection-related mortality in the world that can cause devastating invasive infections like necrotizing fasciitis and serious immune complications like toxic shock syndrome, glomeruloronephritis, and rheumatic heart disease. Despite this pathogens prevalence and potential severity, a safe and effective vaccine is not yet available. GAS pharyngitis (strep throat) is common and typically highly responsive to antibiotics, making is a leading indication given for antibiotic prescription in the United States and worldwide (pharyngitis’s typically viral etiology notwithstanding).
We recently discovered the ability of GAS to cause severe disease is limited by the host inflammatory cytokine IL-1β. Removal of this immune barrier using anti-inflammatory therapeutics greatly increases the incidence and severity of GAS infection and is a serious adverse effect for these drugs, but restoration of inflammatory signaling is protective. A major interest of ours is therefore identifying how GAS and other pathogens benefit from inflammatory dysregulation and how the host-pathogen interaction can be targeted for the development of anti-infective therapeutics. In some instances, this takes the form of boosting the host antimicrobial immune functions that the pathogen is attempting to evade. Other pathogens thrive off of excessive immune activation, so we are also identifying how to prevent pathological hyperinflammation to better maintain a coordinated and effective immune response.
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