Our research program focuses on the role of immune response in inflammation and metabolism. Our expertise in pathways that regulate innate immunity — developed through the pursuit of studies ranging from reductive analysis of TLR ligand signaling to the role of IL-17 axis in experimental models of obesity and infection — have spearheaded the projects aimed at defining the role of the immune mediators in the development and progression of obesity, obesity-associated sequelae and infection / inflammation driven preterm birth.
Recently we have illustrated, to our knowledge, the first evidence for a critical role for IL-17 axis in driving nonalcoholic fatty liver disease (NAFLD) progression, as well as the first report of a role for microbe-driven IL-17 production in exacerbating hepatocellular damage in NAFLD. Current studies are focused on defining the cellular and molecular mechanisms underlying the regulation of NAFLD pathogenesis by the IL-17 axis. Further, we have recently shown that housing animals at thermoneutrality significantly alters animal physiology, immune response and more human-like disease development in mice — something that may allow for better interrogation of cellular and molecular mechanisms underlying disease pathogenesis.