Treatments for fever without the adverse side effects of current medication may be on the horizon, suggests a paper in the November issue of Nature Neuroscience. The study identifies a key enzyme in the chemical pathway in the brain that triggers fever, and proposes that drugs targeting this enzyme could provide improved fever control.
In response to inflammation or infection, cells in the blood vessel walls release a chemical called prostaglandin E2 (PGE2), which acts on the brain to induce fever. Current drugs target and inhibit the function of cyclooxygenase, an enzyme involved in the production of prostaglandins, including PGE2. But prostaglandins have a number of functions and blocking them all might be the reason that some current drugs cause unwanted side effects. Researchers have now identified another enzyme, mPGES-1, involved more specifically in the production of PGE2. When the researchers injected mice that lacked the mPGES-1 gene with a toxin to induce fever, PGE2 levels did not increase, and body temperature was normal. Thus, mPGES-1 appears to be an important ‘switch’ for activating the fever response.
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