Dr. James Bayrer is an Assistant Professor of Pediatrics at the University of California, San Francisco. As a practicing pediatric gastroenterologist and physician scientist, his work focuses on the mechanisms underlying diseases like inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). IBD is a multisystem problem, sitting at the intersection of the immune system, the microbiome, and the intestinal epithelium—he has focused his career on studying the latter. During his early work, he studied Liver Receptor Homolog-1 (LRH-1), a nuclear hormone receptor. He found that LRH-1 is critical for GI development and epithelial renewal. His team discovered that LRH-1 knockout in mice induces intestinal inflammation due to increased apoptosis and decreased Notch signaling. Using mouse and human organoids, he found this is a conversed mechanism. He further showed that overexpression of LRH-1 is protective against harsh chemotherapeutics and inflammatory molecules. To further investigate the role of the intestinal epithelium in health and disease, he collaborated with Dr. Nick Bellono on a landmark paper establishing that enterochromaffin cells form functional synapses with sensory nerve fibers, and that enterochromaffin cell activation triggers visceral mechanical hypersensitivity— a feature of IBS. Interestingly, in looking again at LRH-1, he found LRH-1 knockout mice have disrupted enteroendocrine and enterochromaffin cell development. In fact, his preliminary data show LRH-1 knockout mice demonstrate visceral hyposensitivity despite no change in mechanical compliance or GI transit time. By continuing to investigate this and other molecular pathways, he aims to discover targets to improve the clinical syndromes of IBD and IBS.
See his lab’s webpage here.