Discovery offers hope for new Crohn's disease treatment

Researchers from the University of British Columbia (UBC) have made a discovery which could potentially lead to a treatment for a debilitating complication of Crohn's disease.

Crohn's disease is an inflammatory bowel disease which can affect any part of the gastrointestinal tract, with symptoms including abdominal pain, diarrhoea, fever and weight loss. In some patients, the intestines can become blocked by thickened and scarred connective tissue – a condition known as fibrosis. When fibrosis occurs, surgery is required to restore normal digestion. It is not uncommon for some patients to undergo repeated surgeries.

In their research, published in the journal Science Immunology, scientists discovered a mutation that prevented mice from developing fibrosis after they were infected with a type of salmonella which mimics the symptoms of Crohn's. The mutation in the mice 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," explained co-author of the study Kelly McNagny, a professor of medical genetics at UBC. "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."

McNagny and the UBC team are hopeful that their discovery could be applied to other types of tissue that experience fibrosis.

"Fibrosis is a response to chronic inflammation, but it is also a process that occurs during normal ageing. If you can reverse this, you've essentially found a way to promote regeneration rather than degeneration," stated lead author Bernard Lo, a PhD candidate at BRC.

McNagny points out that liver cirrhosis, chronic kidney disease, muscle degeneration and scarring from heart attacks all result in tissue fibrosis. "We think that we can potentially block complications of all these age-related fibrotic diseases by dampening these particular inflammatory cell types," he concluded.

The next step for the team will be to test drugs, based on the discovery, to ascertain whether they can stop fibrosis in mice.