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amyeoconnell

WNT2B Prevents Intestinal Inflammation

Updated: May 5


In late April, our most recent original research was accepted for publication in the journal Cell and Molecular Gastroenterology and Hepatology (CMGH). This journal is published by the AGA, the largest society for gastroenterologists in the US. It is a journal that features mechanistic studies that relate to intestinal and other GI disorders. You can check out the paper here:



Why is this paper important?

Several human diseases of the intestine (small intestine or colon) involve the development of inflammation, or unchecked production of molecules that cause swelling, increased blood flow, and tissue injury. One disease like this is ulcerative colitis, which affects millions of people worldwide and affects the colon. In our previous study, we found that people with mutations that cause them to not make functional WNT2B protein also have chronic inflammation. In this paper, we show directly that loss of WNT2B leads to chronic inflammation, particularly in the colon. When WNT2B isn't present, the colon has increased levels of proteins called cytokines, that can cause the body's immune cells to be activated or call them to collect at a particular site. The finding that low WNT2B increases inflammtion suggests that higher levels of WNT2B may prevent inflammation, however, this is not a sure thing because for some molecules both high and low amounts can be bad - there has to be a "just right" Goldilocks amount. We will be doing additional studies in the lab to test this. If increasing WNT2B can protect the intestine, that this might be a new approach to treating inflammatory diseases of the intestine, like ulcerative colitis.



Figure: A colon from a WNT2B deficient mouse during colitis.

The cell nucleus is stained blue, the outlines of the epithelial cells that line the colon are in green, and the neutrophils, a cell that is recruited during high inflammation, are red.


Want to Know More?

Please check out a detailed summary of our research findings on Twitter/X: https://twitter.com/AEO_MDPhD/status/1785389202269450267

Feel free to contact us if you have questions, or want to know more!





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