Cytokines, sepsis and the surgeon.

Abstract

Trauma and infection cause complex neuroendocrine responses. Afferent nervous stimuli, stimuli from the central nervous system, local wound factors and endocrine changes characterized by increases in stress hormones are some of these responses. Molecular biology has launched us into an age in which the categorization of these neuroendocrine changes will be broadened to include the profound effects of previously unidentified molecules. TNF and IL-1 are two protein hormones of the cytokine family. TNF causes hemorrhagic necrosis of solid tumors, mediates the lethal effects of endotoxemia and induces immune metabolic and intercellular changes. IL-1 is a mediator of inflammation and the acute phase response. The diversity of actions of TNF and IL-1 appear to be results of their multiple forms (alpha and beta) and their abilities to act both as membrane-associated and free proteins, to act locally (paracrine) as well as systemically, to act synergistically and to be involved in complex webs of self-promotion and amplification. On the basis of these diverse capabilities, they are prime candidates to be mediators of common surgical disease.

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@article{Brown1989CytokinesSA, title={Cytokines, sepsis and the surgeon.}, author={Jamie M Brown and Maddacena Grosso and Alden Hood Harken}, journal={Surgery, gynecology & obstetrics}, year={1989}, volume={169 6}, pages={568-75} }