Abstract
Cytokines are widely believed to mediate the pathophysiology of the systemic inflammatory response syndrome (SIRS) which is associated with sepsis syndrome and the acute respiratory distress syndrome (ARDS) [1]. Cytokines are protein mediators that function as communication molecules by signaling diverse cellular responses. Once thought to be the exclusive product of immune cells, we now realize that both immune and non-immune cells can be stimulated to synthesize and release cytokines. After release, cytokines can act either locally or at a distant site reached through the circulation. Cytokines bind to specific signal-transducing receptors that are located on the cell of origin (autocrine), cells in the immediate vicinity of the cell of origin (paracrine), or on distant cells (endocrine). Receptor binding of cytokines initiates signal transduction through the generation of second messages which result in intracellular signals that include phosphorylation and dephosphorylation of important enzymes, and expression or deactivation of gene products that influence cellular behavior.
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Christman, J.W., Blackwell, T.S., Clark, M.P. (1997). Activation of Nuclear Factor-кB in Sepsis and ARDS. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1997. Yearbook of Intensive Care and Emergency Medicine, vol 1997. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-13450-4_3
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DOI: https://doi.org/10.1007/978-3-662-13450-4_3
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