NEW YORK--(BUSINESS WIRE)--In the September 5 issue of the journal Cell, a group of researchers led by Richard Blumberg, MD, Chief of the Division of Gastroenterology, Hepatology and Endoscopy at the Brigham and Women’s Hospital and Professor of Medicine at Harvard Medical School, together with co-senior investigator Laurie Glimcher, MD, Irene Heinz Given Professor of Immunology and Medicine at Harvard School of Public Health and Harvard Medical School, reported on their discovery of a new genetic risk factor for development of Crohn’s disease and ulcerative colitis - collectively known as inflammatory bowel diseases (IBD). The research team developed an experimental mouse to test the role of a gene called XBP1 as a risk factor for these currently incurable digestive diseases affecting millions of people around the world. In the mouse model, they deleted the XBP1 gene within the epithelium—those cells that line the intestine. The epithelium is the front line for immunologic response to the billions of bacteria that reside in the intestine. The experimental mice with the missing gene spontaneously developed an intestinal inflammation that resembled IBD. The study demonstrated how the lack of the XBP1 gene disabled the normal communication between intestinal epithelial cells and gut bacteria, resulting in dysfunctional immune response and disease.
