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Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

Over the last decade, numerous basic biological as well as experimental and clinical studies have firmly established the significance of tumor necrosis factor (TNF) as a principal proximal mediator of sepsis. Originally identified as a tumoricidal agent, TNF is now recognized as a major inflammatory cytokine with pleiotropic activities on many cell types and organs, which is involved in the local physiological host immune response to invading micro-organisms as well as in the pathophysiology of systemic inflammatory conditions, such as sepsis [1–4]. Highly elevated systemic levels of TNF, as observed during sepsis and septic shock, induce a wide range of immunological and metabolic sequelae, that result in tissue injury, eventually culminating in multiple organ dysfunction with high mortality. The accumulated evidence for the central involvement of TNF in the pathogenesis of septic shock has led many researchers, molecular biologists and clinicians alike, to investigate the complex mechanisms that regulate the production and release of TNF, and that determine its biological effects. The goals of such research efforts are to gain more insight into the pathophysiology of critical illnesses, to develop sensitive and rapid diagnostic tests, and ultimately to provide new therapeutic strategies from which the critically-ill may benefit.

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Bouma, M.G., Buurman, W.A. (1999). Soluble TNF receptors. In: Redl, H., Schlag, G. (eds) Cytokines in Severe Sepsis and Septic Shock. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8755-7_7

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  • DOI: https://doi.org/10.1007/978-3-0348-8755-7_7

  • Publisher Name: Birkhäuser, Basel

  • Print ISBN: 978-3-0348-9759-4

  • Online ISBN: 978-3-0348-8755-7

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