2024-01-13 17:00:00
A research team from the Medical University of Vienna (MedUni) discovered what might be the trigger for inflammatory bowel disease (IBD). The discovery might lead to improved therapies for those affected.
VIENNA. Up to 80,000 people in Austria suffer from chronic inflammatory bowel disease (IBD). IBD refers to chronic, inflammatory, non-contagious diseases of the digestive tract. Chronic inflammation in the intestines is associated with recurring complaints in the digestive tract for those affected, which can sometimes massively restrict everyday life. It is typical for flare-ups to alternate with symptom-free phases.
Until now, the cause of the two most common forms of IBD, Crohn’s disease and ulcerative colitis, was not known. Therefore, the treatment of sufferers has so far been aimed at alleviating the symptoms that are often associated with pain. But that might change soon.
On the trail of the cause
As announced, a research team from the Medical University (MedUni Vienna) was on the trail of the cause of IBD – and may have discovered the trigger. The researchers identified the possible cause of Crohn’s disease and ulcerative colitis on the surface of intestinal epithelial cells.
In their experiments, the research group led by Bernadette Mödl and Robert Eferl from the Center for Cancer Research (ZKF) and the Comprehensive Cancer Center (CCC) at MedUni Vienna were able to show for the first time that certain changes in the brush border of intestinal epithelial cells might be linked to the development of IBD. The brush border consists of dense, finger-shaped projections (microvilli) on the surface of the intestinal epithelial cells, the cells of the outermost layer of the intestine. The microvilli are connected to each other by a protein complex (intermicrovillar adhesion complex – IMAC for short), which is responsible for an ordered structure of the brush border.
Missing protein
It has been known for some time that a certain protein from the IMAC (CDHR5) is present in reduced levels in people with IBD. In order to explore the previously unknown connections, the research team created a mouse model in which CDHR5 was missing. As shown by electron microscopy, the microvilli in the brush border of these mice appeared shortened and completely disordered, like unkempt hair.
“But that alone did not lead to the penetration of harmful bacteria and the development of an intestinal infection,” reports first author Mödl. IBD only occurred following the protective mucous layer over the intestinal epithelial cells was made permeable as part of the experiment.
Attributed to unhealthy diet
“Reduced or missing IMAC protein and the associated organizational deficit in the brush border, in combination with the permeability of the mucous layer, have been found to be a possible trigger for chronic inflammatory bowel disease,” says study leader Eferl, summarizing the results. Accordingly, active ingredients that promote the production of IMAC proteins in intestinal epithelial cells might represent a possible starting point for the development of a causal therapy for IBD.
The fact that unhealthy, high-fat food is associated with the development of IBD can also be explained by the current study results, it is said. This diet would demonstrably make the mucous layer in the brush border of the intestinal epithelial cells more permeable. This might be particularly critical for people who have a family history of low production of CDHR5, according to the researchers.
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