Though FGF10 is known to reduce the severity of DSS-induced colitis and inhibited LPS-induced cell death and pro-inflammatory cytokine secretion in our mouse model, its role in NEC models and how it may protect the intestinal lining is still unknown. Therefore, we will test the hypothesis that FGF109 enhances cell survival and decreases inflammation following insults in the small intestine in a mouse model of endotoxemia and a rat model of NEC.

To test this hypothesis, we will (1) test the effect of different concentrations of FGF10 on the severity of NEC in neonatal rats (2) determine the presence and amounts of FGF10 in human breast milk, allowing to identify a novel growth factor with potential therapeutic and/or preventive use for NEC.

NIH Funding Acknowledgment: Important - All publications resulting from the utilization of SC CTSI resources are required to credit the SC CTSI grant by including the NIH funding acknowledgment and must comply with the NIH Public Access Policy.