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

Abstract

Sepsis/septic shock results from the excessive activation and release of a number of inflammatory mediators. Cytokines are generally considered to be key factors in this respect as these hormone-like proteins are released in excessive amounts during sepsis and are able to induce the release and activation of a number of secondary and tertiary mediators [1]. The main cytokines involved in the pathogenesis of sepsis are tumor necrosis factor-α (TNFα), interleukin-lα, -β(IL-lα/β) and interleukin-1receptor antagonist (IL-1ra), IL-6, IL-8 and other chemokines, IL-10, IL-12, and interferon-gamma. Among the secondary mediators activated by cytokines are plasma cascade systems such as the coagulation, fibrinolytic and contact systems. These systems have in common that during activation proenzymes are converted into active serine proteinases in a waterfall or “cascade”-like fashion. In this chapter we will first discuss some aspects of the biochemistry and biology of these systems. Then we will elaborate on the role of cytokines in the activation of clotting and fibrinolysis, in particular during sepsis. Finally, we will summarize possible effects of clotting or fibrinolytic proteins on the release of cytokines.

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Hack, C.E. (1999). Cytokines, coagulation and fibrinolysis. 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_11

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  • DOI: https://doi.org/10.1007/978-3-0348-8755-7_11

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