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Stephan Targan, MD
Robert Barrett, PhD
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder primarily affecting the gastrointestinal tract and is believed to be caused by dysregulated immune responses to bacteria in genetically predisposed individuals.
Our mission in the Gut Program at the Cedars-Sinai Regenerative Medicine Institute is to understand how genetic defects in intestinal epithelial cells contribute to the development of IBD. In so doing, we aim to improve the treatment and prevention of the disease.
IBD affects approximately 1.4 million Americans. There are two major forms of IBD: Crohn’s disease, affecting any part of the gastrointestinal tract, and ulcerative colitis, affecting the innermost lining of the large intestine.
Our focus is on gene mutations within the intestinal epithelium — the innermost lining of the intestine — and how these mutations either cause or assist the development of IBD. Defects in intestinal epithelial cells play a role in the pathogenesis of IBD. However, as these cells are greatly influenced by intestinal bacteria and the host immune system, it is extremely difficult to develop a proper model of IBD in a culture dish.
The Gut Program, based in the lab of Robert Barrett, PhD, is the first to culture human intestinal epithelium carrying mutations related to the pathogenesis of IBD. Immune cells from individuals with IBD can be converted into iPSCs that are then directed to form three-dimensional intestinal organoids composed of all the epithelial cell types found within the human intestine. These complete intestinal organoids can be used to study how the genetic mutations affect the intestinal epithelium and contribute to IBD. They also have the potential to be used for novel drug screening.
The Gut Program scientists collaborate with the Inflammatory Bowel Disease Center and the F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute. Through this collaboration, researchers have access to the immune cells of more than 10,000 patients with IBD.