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Hirschsprung’s Disease (HSCR) patients that develop Hirschsprung’s-associated Enterocolitis (HAEC) have worse long-term bowel function than those that never develop HAEC, possibly secondary to inflammatory changes to the enteric nervous system (ENS). A functioning ENS, which controls motility, water and nutrient absorption, and local blood flow, is essential to life. Common gastrointestinal diseases in the pediatric population, such as anorectal malformations, intestinal atresias, and motility disorders are associated with disturbances in basic ENS functions, and are likely associated with subtle, underappreciated, anatomic changes in the ENS as well as mucosal immune system.

Additionally, recent evidence indicates that there are perturbations in ENS form and function in the setting of inflammatory bowel disease-related colitis, as well as age- and severity of disease-related declines in ENS function in diabetes mellitus. Taken in this context, Hirschsprung’s disease can be considered a forme fruste of enteric nervous system dysfunction and is an ideal model system for studying gastrointestinal immune function in the presence and absence of the ENS. The long-term goal of our research is to gain an understanding of the interactions between the Enteric Nervous System and Gastrointestinal Immune System in both development and disease to permit the generation of novel neuro-immunomodulatory therapies that may potentially target a broad range of congenital and acquired pediatric gastrointestinal tract diseases (Hirschsprung’s disease, Necrotizing Enterocolitis, Intestinal Atresia, Motility Disorders, Inflammatory Bowel Disease, etc.)


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