Discovery May Lead to New Treatments for Crohn's Disease


Mutation prevents the development of fibrosis in disease that mimics inflammatory bowel disease.

Using a mouse model, researchers may have identified inflammatory cells that drive fibrosis in Crohn’s disease.

In a study published in Science Immunology, researchers used mice infected with a type of salmonella that mimics the symptoms of Crohn’s disease. They found that a mutation prevented fibrosis from developing after the mice were infected.

In fact, the mutation switched off a hormone receptor responsible for stimulating part of the body’s immune response, according to the study.

“We found what we think are the inflammatory cells that drive fibrosis,” said study co-author Kelly McNagny. “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 believe these inflammatory cells may be the orphan nuclear receptor ROR alpha, and the group 3 innate lymphoid cells. In addition to those findings, researchers also believe their discovery could be used with 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,” said lead study author Bernard Lo. “If you can reverse this, you’ve essentially found a way to promote regeneration rather than degeneration.”

Several conditions, such as chronic kidney disease, scarring from heart attacks, muscle degeneration, and liver cirrhosis 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,” McNagny said.

Researchers noted that the next step will be to test different drugs to find out if they can stop or reverse fibrosis in mice.

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