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With intestinal inflammation such as Crohn's disease and ulcerative colitis, positive stress protects the intestine. A new study has now found that the same signals that damage the intestinal wall can also protect it. That means: Inflammatory bowel diseases arise when the balance tilts.
Crohn's disease and ulcerative colitis
Inflammatory bowel disease is increasing. Genetic systems play a role here, as do nutrition, viruses and bacteria. Earlier studies showed that a disorder of the membranes of the endoplasmic reticulum (ER) has an important influence in the genesis of the inflammation.
Persistent diarrhea and extreme abdominal pain
Around 500,000 people suffer from Crohn's disease in Germany, and the number of sufferers is increasing. Above all, the intestinal walls are damaged, which ignite to a great extent. Symptoms include extreme abdominal pain, fever, and chronic as well as severe diarrhea. Those affected can not design a normal everyday life.
Blood stool and fever
Bloody stool mixed with mucus and with a liquid consistency is typical of ulcerative colitis. In the episodes of the disease, those affected can hardly leave the toilet, physical weakness, fever and abdominal pain are added.
ER stress as damage
The phenomenon known as ER stress causes inflammatory messenger substances to form and cells to die. As a result, the intestine can no longer act as a barrier.
ER stress as protection
A new study by Brigham and Women's Hospital at Harvard Medical School has now found that the same signals can do the opposite: instead of destroying cells, they protect the intestine.
Defense cells change into the intestinal mucosa
The positive effect arises when certain defense bodies migrate from the abdominal cavity into the intestinal mucosa. By producing antibodies of the form immunoglobulin A (IgA), they now strengthen the mucous membrane and strengthen its protective barrier. Instead of causing inflammation, they protect against it.
Genetically modified mice
The scientists examined mice that were modified so that ER stress developed in their intestinal mucosa. These animals had one thing in common: the amount of antibodies was significantly increased.
Antibodies in the gut itself
These IgA antibodies are the only antibodies in the intestine themselves and provide a protective layer inside the intestinal surface. If the antibodies were now inhibited in the experiment or if their production was prevented, the protection was not formed - this increases the risk of intestinal inflammation.
Mice and humans
The results cannot be transferred directly because mice are not human. But the insight remains: stress reactions of the cells in the intestine can be just as damaging as building up protection. For future studies, the question now arises as to whether and when this protection is reversed in humans, according to a study employee, Professor Philip Rosenstiel from the Institute for Clinical Molecular Biology at the CAU and board member of the PMI Cluster of Excellence. If this point were found, this could open up completely new approaches to treat inflammatory bowel diseases. (Dr. Utz Anhalt)