What is it about?
We studied the role of platelet activation in the development of colitis in mice. To realize this aim, we generated a mouse with a specific deletion of cyclooxygenase(COX)-1 in platelets which imitates the effect of low-dose aspirin (an antiplatelet agent which acts by selectively blocking the activity of platelet COX-1). These mice were treated with DSS to develop colitis as a consequence of intestinal epithelial damage. The inhibition of platelet function in these mice translated into a milder inflammatory response in the acute phase of the disease associated with a fast recovery. In conclusions, platelets act as inflammatory cells which crosstalk with cells of the stroma, including myofibroblas and immune cells leading to chronic inflammation and fibrosis.
Photo by manu schwendener on Unsplash
Why is it important?
The results of this work help to clarify the mechanisms associated with colitis development and suggest the possible use of antiplatelet agents in the treatment of colitis and intestinal fibrosis. However, this hypothesis has to be tested in patients.
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This page is a summary of: Platelet-Specific Deletion of Cyclooxygenase-1 Ameliorates Dextran Sulfate Sodium–Induced Colitis in Mice, Journal of Pharmacology and Experimental Therapeutics, June 2019, American Society for Pharmacology & Experimental Therapeutics (ASPET), DOI: 10.1124/jpet.119.259382.
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