Researchers help the body protect itself against inflammation and colon cancer

From Virginia Tech:

IMAGE: Coy Allen, (left) an assistant professor of inflammatory disease in the Department of Biomedical Sciences and Pathobiology in the Virginia-Maryland College of Veterinary Medicine, and doctoral student Daniel Rothschild prepare… view more

Credit: Michael Sutphin

Could inflammatory bowel disease and colon cancer be prevented by changing the shape of a single protein?

There is an intimate link between uncontrolled inflammation in the gut associated with inflammatory bowel disease and the eventual development of colon cancer. This uncontrolled inflammation is associated with changes in bacteria populations in the gut, which can invade the mucosal tissue after damage to the protective cellular barrier lining the tissue.

But Virginia Tech researchers found that modifying the shape of IRAK-M, a protein that controls inflammation, can significantly reduce the clinical progression of both diseases in pre-clinical animal models.

The altered protein causes the immune system to become supercharged, clearing out the bacteria before they can do any damage. The team’s findings were published in eBioMedicine.

“When we tested mice with the altered IRAK-M protein, they had less inflammation overall, and remarkably less cancer,” said Coy Allen, an assistant professor of inflammatory disease in the Department of Biomedical Sciences and Pathobiology in the Virginia-Maryland College of Veterinary Medicine and a Fralin Life Science Institute affiliate.

The next step, he said, will be to evaluate these findings in human patients through ongoing collaborations with Carilion Clinic and Duke University. The team is also evaluating their findings in laboratory-assembled ‘mini-guts’–live tissue models that Allen and his team assembled by growing intestinal stem cells on petri dishes to form highly complex small intestinal and colon tissue.

“Ultimately, if we can design therapeutics to target IRAK-M, we think it could be a viable …

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