A group of researchers at the Cincinnati Children’s Hospital Medical Center has reconstructed the events and pathways at the cellular level that predispose to inflammatory bowel diseases, such as Chron’s disease and ulcerative colitis. The study was published in the Journal of Experimental Medicine.
06 APR – A study conducted by a group of scientists from the Cincinnati Children’s Hospital Medical Center (USA) has identified the mechanism that would lead to the excessive inflammatory response that damages the intestine, causing the appearance of inflammatory bowel diseases such as Crohn’s disease and colitis ulcerative.
The team conducted several experiments to understand how the immune cells of the gut detect and respond to microbes and transmit important signals to the epithelial cells of the gut. When this signaling network between immune and epithelial cells is functioning properly, the immune system lives in harmony with the ‘good’ bacteria in the gut.
However, when this exchange of signals is altered, due to genetic mutations or damage to the intestinal epithelium, the immune system may not react or react too much, causing inflammatory bowel disease.
The study by the team of the Cincinnati Children’s Hospital Medical Center (USA) has highlighted how the microbes are detected by the immune cells of the intestine which thus induce the inflammatory cytokine IL-1.
This, in turn, increases the levels of another protein, IL-22, which, together with IL-1, activates the latter’s receptor, expressed on the epithelial cells of the intestine.
Activation of this receptor induces the activity of the ROS gene along with that of other genes that recruit inflammatory cells at the tissue level. This chain reaction leads to an excessive inflammatory response that can damage the gut, the researchers concluded.
Source: Journal of Experimental Medicine 2023
April 06, 2023
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