Altered immunologic responsiveness is a cardinal feature of the syndrome of multiple organ failure (MOF). The mechanisms of immune dysfunction in MOF are largely unknown. Moreover, it is increasingly controversial whether the major clinical consequence of this dysfunction is immunosuppression resulting in enhanced susceptibility to infection and suggesting a need for therapies to stimulate the immune response [1, 2] or overactivity of the immune response with tissue injury the result of systemic activation of the inflammatory response, and a corresponding need for therapies to downregulate the endogenous response [3–5]. It is apparent, however, that alterations in normal immunologic homeostasis play a central role in the pathogenesis of the syndrome.
CITATION STYLE
Marshall, J. C. (1993). Immunologic Dyshomeostasis in Multiple Organ Failure: The Gut-Liver Axis. In Host Defense Dysfunction in Trauma, Shock and Sepsis (pp. 243–252). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-642-77405-8_26
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