Gosain Lab

Our laboratory focuses on two fundamental aspects of the Enteric Nervous System (ENS). The ENS, or “brain-of-the-gut,” controls motility, secretion, digestion, and absorption in the entire gastrointestinal tract and is essential to life. Common enteric neuropathies, including Hirschsprung Disease (HSCR), esophageal achalasia, gastroparesis, enteric dysmotility, and chronic intestinal pseudo-obstruction, result from congenital defects in ENS development or from acquired loss of enteric neurons due to infection, immune-mediated inflammation, or neuronal degeneration, and cause significant gastrointestinal morbidity in children and adults.

Cell-Based Therapies for Enteric Nervous System Regeneration

We have a specific interest in developing cell-based therapies to generate or regenerate a missing or dysfunctional ENS. During development, Neural Crest Cells (NCC) which populate the GI tract to form the ENS, integrate multiple signals from their surrounding intestinal microenvironment to survive, proliferate, migrate, and differentiate. These interactions are governed primarily through receptor-ligand interactions of NCC with their surrounding extracellular matrix (ECM). Our goals are to define the molecular mechanisms of NCC interactions with ECM in order to develop a personalized medicine, cell-based therapeutic approach to enteric neuropathies.

Intestinal Homeostasis and Gut-Brain-Immune Interactions

Intestinal homeostasis is governed by dynamic communication between the lining of the intestine (epithelium), the “brain of the gut” (ENS), the immune system of the gut (mucosal immune system) and the bacteria that live in the gut (microbiota). Perturbations in this four-way intestinal homeostatic crosstalk underlie a broad range of both congenital and acquired diseases, including necrotizing enterocolitis (NEC), Hirschsprung-associated enterocolitis (HAEC), inflammatory bowel diseases (IBD, both Crohn’s disease and Ulcerative Colitis), and many others. A critical barrier in the field is that the precise mechanisms by which the ENS contributes to maintenance of intestinal homeostasis remain poorly defined. Our group is working to define these mechanisms in order to develop novel prevention strategies and therapies for inflammatory conditions of the GI tract.