A paradox helps explain how aspirin works


Putting the pieces of the puzzle together, Casolaro and his team embarked on a study to test the notion that aspirin might actually increase IL-4 production using T cells from healthy donor blood and culturing them in the presence of aspirin. To his surprise, aspirin significantly reduced IL-4.

"The bottom line was a paradox," he says. "We found that aspirin had the opposite effect of what we might have expected and was clearly acting in a completely novel way." In mapping the gene responsible for the production of IL-4, they found that aspirin targets part of a complex of DNA binding proteins that form on the IL-4 promoter, the region that regulates the quantity of protein manufactured.

"Before this study, we knew that, fundamentally, aspirin had at least two pathways of action, on COX and on NF-ΚB. This study is the first evidence that aspirin influences IL-4, and does so via a third, novel pathway," says Casolaro.

The researchers speculate that because IL-4 favors recruitment of inflammatory cells from the blood stream, a process implicated in rheumatoid arthritis and heart disease, suppressing IL-4 with aspirin may be one reason the drug protects against both conditions.


Contact: Kate O'Rourke
Johns Hopkins Medical Institutions

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