A new discovery could lead to the development of treatments for Crohn's disease and its debilitating complications.

Crohn's disease is a bowel disease characterized by the inflammation of the intestines, particularly the colon and ileum, and is commonly associated with ulcers and fistulae. In some patients, the intestines are blocked by thickened and scarred connective tissue -- a condition known as fibrosis. Patients suffering from fibrosis would typically need surgery to restore proper digestion.

In a study published in Science Immunology, scientists from the University of British Columbia (UBC) were able to prevent the development of fibrosis in laboratory mice after infecting them with a type of salmonella bacteria that mimics the symptoms of Crohn's disease. According to the researchers, the mutation that prevented fibrosis had switched off a hormone receptor responsible for stimulating the immune response in some parts of the body.

"We found what we think are the inflammatory cells that drive fibrosis," Kelly McNagny, professor of medical genetics, co-director of the UBC Biomedical Research Center and co-author of the study, said in a statement. "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."

The researchers also hope that the discovery could also be applied to other types of tissue that could be affected by fibrosis. According to the scientists, other conditions that could lead to tissue fibrosis include liver cirrhosis, chronic kidney disease, scarring from heart attacks and muscle degeneration.

"Fibrosis is a response to chronic inflammation, but it is also a process that occurs during normal aging," Bernard Lo from UBC Biomedical Research Center and lead author of the study, said in the same statement. "If you can reverse this, you've essentially found a way to promote regeneration rather than degeneration."

According to the researchers, the next step would be to test and determine whether certain drugs could prevent or reverse fibrosis in laboratory mice.