The proportion of people suffering from gluten intolerance has almost doubled in the last 25 years. An international team of researchers has now come a step closer to understanding the exact mechanisms behind the disease.
People who suffer from celiac disease have to do without many things: wheat, rye and barley, for example, contain the protein gluten, which is harmful to them, and they cannot digest it. The autoimmune disease is currently considered incurable and can only be treated to a limited extent. The only way to prevent stomach pain and vomiting is to follow a gluten-free diet, which is usually complicated to implement and not particularly nutritious. If celiac disease is not diagnosed, the intestinal villi gradually atrophy, which results in a reduction in the intestinal surface area and thus in nutrient absorption.
But considering that on average one in every 100 people in Germany is affected by gluten intolerance, surprisingly little is known about the exact course of the disease. For example, it was long assumed that the inflammatory reactions occur when immune cells in the intestinal wall react to the gluten proteins. But an international team led by Sara Rahmani from McMaster University in Canada has now, after six years of intensive research, managed to better understand the processes of gluten absorption in the body.
To find out how the intestines of celiac patients deal with gluten, they developed organoids from biological materials that act as a model of the inner intestinal wall. One such organoid can also be seen in the picture. These structures, which are just a few millimeters in size, consist of cells of one type of tissue and exhibit organ-like properties. With their help, the scientists were able to study under controlled laboratory conditions what role certain intestinal molecules play in food intake, something that is almost impossible in a living organism.
What the research group discovered confirms a hypothesis that has been put forward for some time: cells of the intestinal epithelium, i.e. the inner intestinal mucosa, alert the body’s immune cells in celiac patients when they come into contact with gluten. The immune system is therefore activated when the gluten interacts with the intestinal surface and not only when it has almost passed the intestinal wall. The receptors of the intestinal epithelium evidently play an important role in the inflammatory cascade of gluten intolerance, which at the same time offers a starting point for future medications. By precisely localizing the immune response, it could be easier to search for targeted treatment options in the future.