Dr. Mannon's translational research in IBD has focused on improving current treatment responses by studying endophenotypes of disease to predict efficacy of approaches and testing novel, or re-purposing existing, drugs for inflammatory bowel disease (IBD). An overarching point of reference for his research program is the gap between response and non-response to conventional and experimental treatments. This perspective has allowed Dr. Mannon and his collaborators to show how IL-10 production and infiltration of the lamina propria with suppressor-inducing plasmacytoid dendritic cells conferred clinical response from G-CSF therapy in Crohn’s disease (while non-responders showed neither finding) and also how high IL-17 production could prevent (predict) lack of clinical response to interferon-beta in ulcerative colitis (UC).  Current research projects are focused on defining endophenotypes of IBD that can predict enhanced responses to highly targeted therapeutic agents, specifically anti-IL-13, anti-IL-17, and anti-TNFa in treating UC as well as identifying the microbial-antigen reactivity of highly shared TCRβ CDR3 clonotypes in Crohn’s disease which has become the basis for a long-term project to develop T cell-based immunotherapies for Crohn’s disease.

Dr. Mannon has served as the GI Site expert on the Human Microbiome Project, involved in the early stages of protocol planning and at the final stages of data analysis. His expertise in this area supported projects on the role of gut microbiome in solid organ transplant-associated metabolic syndrome and microbiome effects on Barretts esophagus.  He has significant experience in designing and executing investigator-initiated studies as well as sponsored studies.  He has extensive experience in translational research in inflammatory bowel disease and mucosal immunology, and specific experience in the role of biologic agents in gut epithelial and mucosal immune response as well as a specific interest in the mechanism of inflammation in IBD.