Chronic inflammatory bowel diseases, like Crohn’s disease and ulcerative colitis, can be painful and disruptive, especially for young people.
These diseases often appear between the ages of 15 and 29—a time when many are finishing school, starting work, and planning their future. People living with these conditions can suffer from severe stomach cramps, diarrhea, weight loss, fatigue, and stress.
These symptoms come and go in waves, known as flare-ups. In serious cases, long-term inflammation can damage the intestines and increase the risk of bowel cancer.
Ulcerative colitis affects only the inner lining of the large intestine, while Crohn’s disease can go deeper and show up in any part of the digestive system, including the small intestine, stomach, and esophagus.
Treatments have traditionally focused on calming down the immune system to reduce inflammation, but not everyone responds well to these therapies. New, more targeted treatments aim to block specific immune system signals that cause inflammation. And now, researchers in Germany may have found a key piece of the puzzle.
At Charité – Universitätsmedizin Berlin, Professor Ahmed Hegazy and his team have been studying how the immune system behaves in the gut. They’ve made an important discovery: two immune messengers—interleukin-22 (IL-22) and oncostatin M (OSM)—work together in a harmful way to fuel inflammation.
IL-22 usually helps protect the gut lining, while OSM is involved in healing tissues. But in people with chronic bowel disease, these two substances start working together in a way that makes the inflammation worse.
Professor Hegazy explained that many of their patients are young adults whose lives are seriously impacted. Some of these patients don’t respond to the usual medications, and the team noticed that people with high levels of OSM often fall into this group.
This led them to wonder: could OSM be a sign of more serious illness? Could it help doctors predict who won’t benefit from current treatments?
Over five years, the researchers studied both animals and human tissues to learn more. Using advanced technology, they looked at each individual cell to see what was going on. They found that inflamed guts had many more cells with receptors that respond to OSM.
Even more surprising, IL-22 made things worse by increasing the number of OSM receptors—almost like adding fuel to a fire. As the two messengers teamed up, more immune cells were drawn into the gut, making inflammation spread.
When the team blocked these OSM receptors in their models, inflammation went down—and so did signs of cancer.
The researchers also looked at tissue from patients with colon cancer caused by long-term bowel inflammation. They saw large numbers of OSM receptors near the tumors, but not in healthy areas. This suggests that OSM might play a role in turning inflammation into cancer.
Still, not everyone with inflammation will get cancer—every patient is different. That’s part of what makes treating these diseases so hard.
Professor Britta Siegmund, head of the clinic where the study took place, says that these findings give researchers a much clearer idea of what’s driving the disease in some patients. By understanding how IL-22 and OSM work together, scientists can now look for ways to block this harmful cycle.
This exciting research is already being put into action. A new clinical trial is underway to test an antibody that blocks OSM receptors. If successful, this therapy could offer relief to patients who haven’t responded to older treatments.
By stopping the damaging teamwork between IL-22 and OSM, the goal is to reduce inflammation, prevent long-term damage, and lower cancer risk.
This discovery is a promising step toward better, more personalized treatments for people with chronic inflammatory bowel diseases. With new therapies on the horizon, young people facing these life-altering conditions may finally get the help they need to live healthier, fuller lives.
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The study is published in Nature Immunology.
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