Scientists from the University of British Columbia discovered a mutation that prevented mice from developing fibrosis after they were infected with a type of salmonella that mimics the symptoms of Crohn disease. The discovery could lead to treatments for a debilitating complication of the disease. The mutation had switched off a hormone receptor responsible for stimulating part of the body’s immune response.
Co-author Kelly McNagny, professor of medical genetics and co-director of the UBC Biomedical Research Centre, identified that scientists found what they think are the inflammatory cells that drive fibrosis, adding that the gene that was defective in those cells is a hormone receptor, and that there are drugs available that may block that hormone receptor in normal cells and prevent fibrotic disease. McNagny and colleagues are hopeful that their discovery could also be applied to other types of tissue that experience fibrosis, potentially blocking complications of age-related fibrotic diseases by dampening these particular inflammatory cell types. Liver cirrhosis, chronic kidney disease, scarring from heart attacks, and muscle degeneration all result in tissue fibrosis. The researchers’ next step will be to test drugs to discover if they can stop or reverse fibrosis in mice.
The research, “The orphan nuclear receptor ROR alpha and group 3 innate lymphoid cells drive fibrosis in a mouse model of Crohn’s disease,” is published in the September 2016 issue of Science Immunology and is available online at http://immunology.sciencemag.org/content/1/3/eaaf8864.
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