Scientists identify gut vulnerability during IBD remission — ScienceAlert
A research team from Australia has found that the intestinal lining of people with inflammatory bowel disease may retain cellular vulnerability even when disease symptoms are under control. As ScienceAlert reports, this may partly explain why patients experience flare-ups again after remission.
Inflammatory bowel diseases include Crohn’s disease and ulcerative colitis, among others. Both conditions are associated with chronic inflammation of the digestive tract. Treatment can suppress disease activity, but remission does not always mean that biological processes in the tissues have fully returned to normal.
More than 900 biopsies
The study, published in the journal Science, included more than 900 intestinal biopsies taken from 80 people, some of whom had inflammatory bowel disease. In most patients with IBD, the disease was inactive or had mild activity. The team led by scientists from the Walter and Eliza Hall Institute examined the intestinal lining, which is constantly renewed.
Normally, controlled cell death helps the body eliminate damaged or unnecessary cells, while stem cells produce new ones. The scientists found that inflammation can alter the behavior of intestinal cells and make them more sensitive to abnormal death signals. Some of these signals were detected even in tissues without obvious signs of inflammation.
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Conclusions require verification
For further analysis, the researchers grew organoids — miniature models of intestinal tissue — from human samples. Signals associated with necroptosis, a process of cell death in which contents are released and may intensify inflammation, were found in patient samples. At the same time, in organoids exposed to inflammatory signals, cells mostly died through apoptosis, a more orderly mechanism.
Blocking necroptosis under experimental conditions did not prevent cell death. Deleting individual genes in laboratory conditions protected certain cell types, but the safety of this approach for patients still needs to be studied.
Of 52 patients with IBD, follow-up data over two to three years were available for 30. Sixteen of them experienced a flare-up requiring intensification or a change of treatment, while 14 remained stable. Those who later had a flare-up had higher levels of a cell-death signaling marker than people without IBD. At the same time, the authors stress that these results are preliminary and currently do not make it possible to predict flare-ups in a specific patient.
