Their biosynthesis is significantly increased in inflamed tissue, and they contribute to the development of the cardinal signs of acute inflammation. Prostaglandins (PGs) play a key role in the generation of the inflammatory response. It may be anticipated, therefore, that failure of acute inflammation to resolve may predispose to autoimmunity, chronic dysplastic inflammation, and excessive tissue damage. The usual outcome of the acute inflammatory program is successful resolution and repair of tissue damage, rather than persistence and dysfunction of the inflammatory response, which can lead to scarring and loss of organ function. During the resolution of inflammation, granulocytes are eliminated, and macrophages and lymphocytes return to normal preinflammatory numbers and phenotypes. Once the initiating noxious stimulus is removed via phagocytosis, the inflammatory reaction can decrease and resolve. This process causes the cardinal signs of acute inflammation: rubor (redness), calor (heat), tumor (swelling), and dolor (pain). The acute phase of inflammation is characterized by the rapid influx of blood granulocytes, typically neutrophils, followed swiftly by monocytes that mature into inflammatory macrophages that subsequently proliferate and thereby affect the functions of resident tissue macrophages. Inflammation is an intrinsically beneficial event that leads to removal of offending factors and restoration of tissue structure and physiological function. Inflammation is the immune system's response to infection and injury and has been implicated in the pathogeneses of arthritis, cancer, and stroke, as well as in neurodegenerative and cardiovascular disease. Customer Service and Ordering Information.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).

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