822 - Differential Requirements for Epithelial Mitochondrial Respiration in Ulcer Healing

cells upon adoptive T cell transfer in Rag1 -/- .In DSS and T cell transfer colitis, IEC-specific deletion of MHCII in I-Ab D IEC mice conferred modest protection with significantly less weight loss (p<0.01), and decreased mucosal expression of IFN g (p<0.01) and TNF a (p<0.05).DSS colitis in I-Ab D IEC mice was, however, associated with moderately impaired induction of CD4 + CD25 + FOXP3 + regulatory T cells (Treg) in colonic lamina propria compared to I-Ab fl/fl controls (p<0.05),suggesting epithelial MHCII expression contributes to mucosal Treg induction.Upon C. rodentium infection, I-Ab D IEC showed significantly higher relative C. rodentium abundance (p<0.001) with lowered a-diversity index, number of observed OTUs, on day 6 and 9 post-infection (PI) as compared to control mice, with higher fecal Lipocalin 2 on day 9 (p=0.06).Only 50% of the I-Ab D IEC mice survived 15 days PI.Surviving I-Ab D IEC mice showed a trend towards lower IFN g, IL1b and antibacterial lectin RegIIIg expression, suggesting that epithelial MHCII is important for bacterial clearance. Conclusion:In chemically-induced or T-cell mediated colitis, MHCII on IEC may contribute to inflammation, whereas in infectious colitis, it could play an important role in pathogen clearance.