Proinflammatory effects of NSAIDs

Ironically, while prostaglandins are typically described as mediators of inflammation, these substances exert a wide range of anti-inflammatory effects (Figure 3). For example, prostaglandins are potent inhibitors of the release of tumor necrosis factor a (TNFa) and IL-1 from macrophages, and potent inhibitors of TNFa and platelet-activating factor from mast cells. Prostaglandins also suppress the release of a number of proinflammatory mediators from platelets. On the other hand, NSAIDs, by suppressing endogenous prostaglandin synthesis, can increase the release of a number of proinflammatory mediators from various cells, and can therefore enhance an inflammatory reaction (while simultaneously reducing edema and pain). Prostaglandins have also been shown to be potent inhibitors of adhesion molecule expression on the vascular endothelium (e.g. ICAM-i) and on leukocytes (e.g. CD11/CD18), thereby reducing the ability of leukocytes to extravasate. Conversely, NSAIDs have been shown to increase adhesion molecule expression in some experimental models, and to cause a corresponding increase in leukocyte adherence to the vascular endothelium. Actions such as these might explain the observation that NSAIDs can actually lead to increased tissue injury in some forms of inflammation, as well as some of the adverse reactions to NSAIDs in settings of inflammation (e.g. inhibition of the healing of peptic ulcers). Removal of the immunomodulatory effects of endogenous prostaglandins through NSAID administration may

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