In a mouse model of Crohn’s disease, scientists at the University of British Columbia in Canada have made a discovery that could potentially lead to treatments for a debilitating complication of Crohn's disease. Crohn's disease is an inflammatory bowel disease in which the intestines of some patients can become blocked by thickened and scarred connective tissue--a condition known as fibrosis. When fibrosis occurs, surgical intervention is required to restore proper digestion. Repeated surgeries are not uncommon in Crohn's patients. In research outlined in an article published as the cover story of the September 2, 2016 issue of Science Immunology, scientists discovered a mutation that prevented mice from developing fibrosis after they were infected with a type of salmonella that causes the mice to develop symptoms mimicking those of Crohn's disease. The mutation had switched off a hormone receptor responsible for stimulating part of the body's immune response. "We found what we think are the inflammatory cells that drive fibrosis," said co-author Kelly McNagny, Ph.D., Professor of Medical Genetics and Co-Director of the UBC Biomedical Research Centre (BRC). "The gene that was defective in those cells is a hormone receptor, and there are drugs available that may be able to block that hormone receptor in normal cells and prevent fibrotic disease." What's more is that Dr. McNagny and his colleagues are hopeful that their discovery could be applied to other types of tissue that experience fibrosis. The new article in Science Immunology is titled “"The Orphan Nuclear Receptor ROR Alpha and Group 3 Innate Lymphoid Cells Drive Fibrosis in a Mouse Model of Crohn's Disease." "Fibrosis is a response to chronic inflammation, but it is also a process that occurs during normal aging.
Login Or Register To Read Full Story