In a different study, researchers were able to genetically engineer mice to prevent the expression of the AGR2 gene and discovered that they developed Crohn's-like inflammation. This caused them to link the inflammation in that study to adherent-invasive E. coli, or AIEC, which were found to be bacteria implicated in Crohn's disease. In this study, they were able to connect that changes in the AGR2 activity levels with increases in the bacteria group that AEIC belongs to. They ended up discovering that the inflammation that was kicked off by the interaction was linked to the production of IL-23, an immune signal that is an important driver of inflammatory bowel disease (IBD) and colorectal cancer tumorigenesis and is also an important therapy target.
In my opinion, I find this research interesting in how this research could affect treatment and medication for this type of disease. If Crohn's disease is triggered by AEIC, I wonder if other digestive and bowel diseases could be caused by similar bacteria found in the digestive tract and if this research can be used to do similar experiments on other gut bacteria and digestive diseases.
It's really interesting to see how specific changes in a gene can cause such a negative response and it makes me wonder what can cause the process to be disrupted. I'm curious to see if the data collected from these studies has helped with any contributions to a cure or treatment for Crohn's disease.
ReplyDeleteI am also curious on whenever other digestive-like diseases are present in the presence of the AEIC bacteria.
ReplyDeleteI wonder if these changes could possibly alter changes in other genes as well. If these changes could alter Chron's disease, could it alter other diseases with similar symptoms.
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