Emily J. Onufer, MD, MPH


Washington University in St. Louis (WU)

Short bowel syndrome results from the surgical loss of significant small intestinal length. In response to this loss, an adaptation response occurs in the remaining bowel characterized by increased enterocyte proliferation leading to taller villi, deeper crypts, and an expanded mucosal surface area. The Warner lab has developed a mouse model for short bowel syndrome in which 50% of small bowel is resected and has shown this adaptive response. Recently, we have shown that IDO1, the rate-limiting enzymatic step in converting tryptophan to kynurenine, is upregulated in our resected versus control mouse model. Kynurenine then acts on AhR to eventually produce IL-22, a stimulus for intestinal healing. The overall goal of this project are is to fully understand the process of adaptation and intestinal re-growth. This information is critical for the development of new therapeutic strategies to enhance this process, thereby saving lives of patients with short gut syndrome.