Study Can this messenger cure chronic inflammatory bowel disease?

Crohn's disease: new findings and therapeutic approaches

A German team of researchers has recently made a discovery on inflammatory bowel disease, which can be of great importance both for understanding the pathogenesis and future treatment of those affected. The researchers developed a new approach to treatment, with the aim of curing the inflamed intestinal mucosa. The core of the investigation is a messenger that promotes the regeneration of the intestinal mucosa.

Chronic inflammatory bowel diseases such as Crohn's disease can already occur in young people and represent a significant loss of quality of life. Previous therapeutic approaches can only suppress or stem the disease at best. A research team from the University of Kiel has now been able to identify a messenger substance that has the potential to heal the inflamed intestinal mucosa. In clinical trials, the researchers were able to show that the so-called interleukin 22 promotes the regeneration of the intestinal mucosa and protects against stress reactions. The study results were recently published in the journal "Journal of Experimental Medicine".

Typical symptoms of inflammatory bowel disease are constant abdominal pain and diarrhea. The background to Crohn's disease is complex and still not well understood. A German research team has now come a step closer to deciphering the disease. (Image: underdogsstudios / fotolia.com)

A new drug for Crohn's disease?

"Interleukin 22 is one of the messengers that promote the regeneration of the intestinal mucosa," says Professor Stefan Schreiber, Director of the Kiel Clinic for Internal Medicine in a press release on the study results. In addition, there is evidence that interleukin 22 can protect the intestinal mucosa from certain stress reactions. The messenger substance has already been tested by the researchers in the first phase of a clinical examination.

The answer is hidden in the genes

As the scientists report, the gene ATG16L1 is considered a risk marker for Crohn's disease. In 20 percent of those affected, a change in the gene was observed. The gene ATG16L1 is responsible for some kind of digestion within cells. If the function of this gene is limited, this results in a reduced degradation of aged proteins. This then leads to increased inflammation. Against this background, the research team asked themselves how to protect patients from this reaction.

Does an altered gene reverse the healing effects??

The team tested the messenger interleukin 22 in intestinal epithelial cells, ie the top cell layer on the inside of the intestine. "In principle, interleukin 22 stimulates cell growth and promotes the regeneration of the intestinal mucosa," explains the first author of the study. Konrad Aden from the Institute of Clinical Molecular Biology. However, in mice that did not have a functioning ATG16L1 gene, the opposite was true. Here, interleukin 22 caused a stress response that led to "paradoxical cell death," the experts reported.

Learn to understand inflammatory bowel disease

"This finding initially helps to understand the complex changes in the bowels of chronic inflammatory bowel disease," says Professor Philip Rosenstiel. The researchers were able to show how the desired protective function of interleukin 22 in the presence of a gene change in the gene ATG16L1 reverses into a pro-inflammatory effect.

How can a therapy be developed from this finding??

"In addition to pure regeneration, Interleukin 22 is also involved in cellular programs that control the body's own antibiotics and thus the intestinal flora," says Rosenstiel. Exactly this interplay is disturbed in the case of chronic inflammatory bowel diseases. Here the experts see a possible approach for targeted therapies. Now, studies are to follow people to continue this approach. (Vb)