Inflammation is the physiological process by which vascularized tissues respond to an infectious agent, antigenic challenge, or physical injury. During the inflammatory process, soluble mediators and cellular components work together to contain and eliminate the agents causing physical distress. Although inflammation is crucial to maintaining the health and integrity of an individual organism, both inadequate and excessive immune responses are detrimental to the health and life of the host. When the inflammatory response is impaired, the host may be excessively susceptible to the detrimental effects of microbial or neoplastic disease. When the inflammatory response is poorly controlled, the host may experience significant or excessive tissue damage.

In addition to its local effects, inflammation also triggers a complex series of behavioral, physiologic, and biochemical systemic changes collectively known as the acute phase response (reviewed in Gabay and Kushner (1999)). The acute phase response is characterized by fever, disordered sleep patterns, alterations in metabolism, and changes in the plasma concentrations of a variety of substances (e.g., iron, C-reactive protein, fibrinogen, serum amyloid A, and albumin). Proinflammatory cytokines, including interleukin-6 (IL-6), IL-1P, tumor necrosis factor-a (TNF-a), IFN-y, transforming growth factor-P (TGF-P) and possibly IL-8, are key regulators of the acute phase response, with IL-6 being the chief stimulator of most acute phase proteins (Gabay and Kushner 1999).

Inflammation can be characterized as acute or chronic. Acute inflammation is a complex, tightly regulated, and generally self-limiting process that is critical for defense against pathogenic microorganisms. However, in some situations, acute inflammation does not resolve or self-limit, but instead progresses into a chronic condition. An appropriate equilibrium between proinflammatory and anti-inflammatory mediators is critical for eradication of the antigenic stimulus without progression to a chronic inflammatory state. If foreign antigen is not eliminated (as in chronic infections such as tuberculosis and chronic hepatitis) or the immune response is inappropriately directed against a self-antigen (as in autoimmune disease), chronic inflammation develops. In some situations, the mechanisms responsible for the development of a chronic inflammatory state are not as clearly defined (e.g., aging, type 2 diabetes, obesity, cardiovascular disease).

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