Therapeutic Target Shows Promise in Preventing Cancer Resulting from Chronic Gut Inflammation

When inflammatory bowel disease becomes chronic, it is difficult to treat and comes with the likelihood of various complications, such as the onset of bowel cancer. This disease in its chronic form manifests as Crohn’s disease or ulcerative colitis. These diseases particularly impact young people. Early diagnosis followed by treatment is crucial in these cases.

A recent study whose findings appeared in the Nature Immunology journal has unveiled a therapeutic target capable of significantly putting the brakes on the processes behind the chronic inflammation underlying inflammatory bowel disease.

The research was conducted by a team based at Charite-Universitatsmedizin Berlin. Professor Ahmed Hegazy, together with his team, identified how the interactions between a pair of messenger substances within the immune system acted as a driver for chronic inflammation in the intestine.

One of these messenger substances is interleukin-22 that plays key roles like maintaining the protective barrier inside the intestine and also supporting the functioning of cells lining the gut. The second messenger substance is oncostatin M, a molecule that helps in inter-cellular signaling and is a major player in cell differentiation as well as tissue repair.

Prof. Hegazy explains that new treatments for inflammatory bowel disease are needed since not all patients respond positively when given the existing treatments. Previous studies conducted by Hegazy and his research team found that oncostatin M set off a domino-effect of other pro-inflammation factors, resulting in an excessive response by the immune system.

In this latest study, the researchers found that patients whose levels of oncostatin M were high didn’t respond appropriately to many of the common treatments. This finding suggests that measuring the level of oncostatin M can provide pointers regarding which patients are unlikely to benefit from treatment. It could also help in identifying patients with severe forms of the disease.

The team also found that cells in inflamed guts have more receptors for oncostatin M, including cells that don’t usually have these receptors. The researchers say interleukin-22 increases the sensitivity of the gut lining to oncostatin M by ramping up oncostatin M receptor numbers. This shows that oncostatin M and interlukin-22 collaborate to amplify inflammation in ways similar to fires that spread as a result of accessing additional fuel.

Worryingly, the team discovered that for patients with colorectal cancer, the tumors had unusually high numbers of receptors for oncostatin M yet the normal tissue around the tumor didn’t have a similar level of these receptors. This finding suggests that oncostatin M could be playing a role in cancer development, but requires additional research to validate.

The findings of Hegazy and his team could open the door to future treatments that seek to block the problematic interaction between oncostatin M and interlukin-22 so that the progression of ailments like Crohn’s disease can be halted or even reversed.

Chronic inflammation isn’t easy to treat since so many factors are usually involved, which is why plenty of research needs to be done to uncover all the mechanisms involved. The academia and for-profit entities like Soligenix Inc. (NASDAQ: SNGX) are doing the best they can to develop effective ways to treat patients diagnosed with these conditions.

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