Researchers from the University of British Columbia, Canada, say they have discovered a mutation that could possibly pave way for treatment of Crohn’s disease. The study was conducted on mice that were infected with a type of salmonella that simulates the symptoms of Crohn’s.

Some of those suffering from the disease develop fibrosis, in which connective tissue is thickened and scarred. These patients often undergo surgeries in order restore proper digestion.

Published in Science Immunology journal, the latest study shows that the mutation prevented mice from developing fibrosis. According to the researchers, a hormone receptor that stimulates part of the body’s immune response was turned off.

"We found what we think are the inflammatory cells that drive fibrosis," Kelly McNagny, study co-author said, in a statement released Friday. "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."

Researchers said that the findings could be put use on different types of tissues affected by fibrosis.

"Fibrosis is a response to chronic inflammation, but it is also a process that occurs during normal aging. If you can reverse this, you've essentially found a way to promote regeneration rather than degeneration," Bernard Lo, the study's lead author, said.

McNagny stated that liver cirrhosis, chronic kidney disease, scarring from heart attacks and muscle degeneration lead to tissue fibrosis.

"We think that we can potentially block complications of all these age-related fibrotic diseases by dampening these particular inflammatory cell types," McNagny said.

Crohn's disease, which is one of the two primary forms of inflammatory bowel disease, can result in abdominal pain, diarrhea, weight loss, anemia and fatigue. The disease does not have any cure but medications such as steroids and immunosuppressants are prescribed to patients to slow the progression of the disease.

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