Ibuprofen is commonly used as a pain reliever. The biochemistry of human pain is incredibly complex. But, two prostaglandins (PGE2 and PGI2) play a key role in the sensation of pain. As an article in Pharmacogenet Genomics stated, “PGE2 and PGI2 are proinflammatory prostanoids that enhance edema formation, increase vascular permeability, and promote leukocyte infiltration.” The paper also notes that these prostaglandins also reduce the threshold at which a pain signal is fired, thereby increasing the sensitivity of nerves.
So, how does reducing the presence of pain and inflammation inducing prostaglandins stop a fever? Turns out, PGE2 is the culprit to blame for producing fevers in the body, a physiologic response called pyresis. As the authors explain, “PGE2 is also a primary mediator of pyresis, and its synthesis is triggered in the hypothalamus.” When certain chemicals called pyrogens are present in the hypothalamus, PGE2 production is initiated.
Therefore, ibuprofen eliminates fevers by stopping the production of PGE2 in the hypothalamus, which prevents the brain from sending instructions for fever production to the body. This leads to relief of the sweating and chills that accompany illness.