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Researchers make strides towards treatment of Crohn's disease

Their findings may allow scientists to stop the development of fibrosis

Photo (c) japhoto - Fotolia
New research from the University of British Columbia could allow those suffering from Crohn’s disease to find some relief. Scientists say they may have found the genetic cause of fibrosis, a serious complication of the disease which affects the intestines. Based on their findings, the researchers believe that they can develop therapies which can help prevent this condition.

“We found what we think are the inflammatory cells that drive fibrosis. . . 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,” said Kelly McNagny, co-author of the study.

Crohn's disease and fibrosis

Fibrosis is a condition characterized by the thickening and scarring of tissues within the body. For those with Crohn’s disease, it affects tissues in the intestines and can cause bleeding, cramps, constipation, and a host of other symptoms. Treatment can often require multiple surgeries.

Fibrosis isn’t unique to Crohn’s disease; it can be symptomatic of several different illnesses, injuries, or even just the aging process. As such, finding the cause of the condition could be beneficial to a wide range of patients.

“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,” said Dr. Bernard Lo, lead author of the study.

Reversing fibrosis

The researchers came upon their discovery while observing mouse models. Certain mice in the study were infected with a type salmonella that mimics the symptoms of Crohn’s disease. However, some mice eventually showed a gene mutation that stopped them from developing fibrotic symptoms.

The researchers tracked this development to a hormone receptor that the mutation had “switched off.” They found that the receptor was responsible for stimulating the body’s immune response, which in turn prompted inflammatory cells to go to work.

By blocking this receptor, the researchers say they can halt the work of inflammatory cells and prevent the development of fibrosis. McNagny, Lo, and their colleagues are now working on testing drugs that can help stop or reverse fibrosis in mice models.

The full study has been published in Science Immunology.

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