Grant: Project Grant

Inflammatory bowel diseases (IBD) are chronic, debilitating illnesses. At present, the goal of treatment in IBD is complete healing of intestinal inflammation. However, despite achieving this target, over twenty percent of IBD patients continue to experience chronic abdominal pain, which is a distressing and devastating symptom. Previous research has shown evidence of increased expression of the transient receptor potential vanilloid-1 receptor (TRPV1) in IBD patients with complete intestinal healing; TRPV1 is a key nerve receptor involved in abdominal pain sensation. There is early evidence that disruptions in gut microbes can also change TRPV1 on pain-sensing nerves. The goal of our research is to study the role of gut microbes in the development of chronic pain in IBD and the interaction between gut microbes and TRPV1 on pain-sensing nerves. We will examine this by performing stool transplants from IBD patients with/without chronic abdominal pain or healthy controls into a mouse model. We will characterize gut microbes and their metabolites in both patients and our mouse model. Finally, we will study how microbe-made short chain fatty acids, which are increased in our mouse model and change the activity of pain-sensing nerves, interact with TRPV1. Our research may have a broad impact on the health of patients suffering from IBD as it will give us a greater understanding into the role of gut microbes in pain sensation. This may in turn lead to new strategies, such as the use of stool transplants, targeted therapies against specific microbial products or microbes, and/or the use of pro-/pre-biotics to treat pain in IBD.