Study identifies promising target for treating inflammatory bowel disease and colitis-induced colorectal cancers

Postdoctoral researcher Xingchen Dong (left) and Assistant Professor Ting Fu (right) in the Fu Lab in the UW–Madison School of Pharmacy’s Pharmaceutical Sciences Division.

Postdoctoral researcher Xingchen Dong (left) and Assistant Professor Ting Fu (right) in the Fu Lab in the UW–Madison School of Pharmacy’s Pharmaceutical Sciences Division.

Inflammation in the gut can trigger a doom loop of sorts. The condition messes with the sensitive relationships between food, digestive acids, microbes and the immune system in ways that can promote further inflammation and, sometimes, the eventual growth of tumors.

Scientists at the University of Wisconsin–Madison have identified a promising new target for treatments that could help the millions of people worldwide who suffer from inflammatory bowel disease and related colorectal cancers.

An essential regulator of gut health
Under the guidance of Ting Fu, an assistant professor in the UW–Madison School of Pharmacy, researchers uncovered a previously unknown function of a protein that is central to gut health and implicated in the development of colitis, a severe and chronic form of IBD. A debilitating condition in and of itself, colitis is also linked to an increased risk for colorectal cancer. The team’s findings suggest that the protein is a promising target for future colitis treatments.

The protein is called the farnesoid X receptor, or FXR. It helps control the production of bile acids that digest fats. Working in tandem, FXR and bile acids play several critical roles in maintaining a healthy gut. Together, they help balance gut bacteria, promote a healthy intestinal lining, and influence immune cells called macrophages that patrol the digestive system and ward off pathogens that sneak in with the food we eat.

“This balance can be thrown off when FXR isn’t functioning properly,” says Xingchen Dong, a postdoctoral researcher in Fu’s lab and the study’s lead author.

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