In mouse models of IBD, the tryptophan metabolizing enzyme indoleamine 2,3-dioxygenase 1 (IDO1) has been shown to limit disease severity. Our studies indicate that intestinal epithelial cells are an important source of IDO1 expression in these conditions; however the mechanism remains unknown. We have identified IDO1 expression in goblet cells as well as colocalization with secreted mucin. As mucin is both a physical barrier against bacterial invasion and an energy substrate for luminal microbes, we hypothesized that epithelial IDO1 may limit colitis severity is through enhancement of mucus barrier function.