Status: Funded - Open
Lauren Frazer, MD, PhD
BACKGROUND: Necrotizing enterocolitis (NEC) is a debilitating intestinal disease that impacts approximately 10% of preterm neonates and has up to a 50% mortality rate. Previous studies by our laboratory and others indicate that dysregulated inflammation is central to the development of NEC. GAP: Interleukin(IL)-22 is cytokine that regulates inflammation and promotes epithelial cell regeneration. The role of IL-22 signaling during NEC remains incompletely understood. HYPOTHESIS: We hypothesize that IL-22 signaling attenuates NEC-mediated intestinal inflammation. METHODS: We will utilize our clinically relevant murine model of NEC to determine the role of IL-22 receptor signaling during NEC. RESULTS: Pending. IMPACT: We are working towards the implementation of IL-22 as a treatment for NEC, and the data generated in this proposal will advance our understanding of the mechanisms of IL-22-mediated protection from disease.