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• W1997883951 abstract "Severe and prolonged states of catabolic stress have been shown to have profound effects on the intestinal tract microflora and intestinal function. Gut-derived sepsis is a term used to describe a state of systemic inflammation with organ dysfunction after severe catabolic stress hypothesized to be initiated and perpetuated by the intestinal tract microflora. Popular notions of the mechanism of this process have suggested that stress promotes the translocation of intestinal bacteria or their toxins into the systemic compartment resulting in the release of proinflammatory cytokines which participate in the systemic inflammatory response syndrome. This review is an attempt to redefine the mechanism of gut-derived sepsis by focusing on molecular events that result from host-pathogen interactions within the intestinal tract itself. This evidence-based review posits that gut-derived bacteremia, even with potent nosocomial pathogens, is an event of low proinflammatory potential and, itself, is an insufficient stimulus for the systemic inflammatory response and organ failure state typically seen after severe and prolonged catabolic stress. Mechanisms of this apparent paradox are discussed." @default.
• W1997883951 created "2016-06-24" @default.
• W1997883951 creator A5031563441 @default.
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• W1997883951 date "2003-02-01" @default.
• W1997883951 modified "2023-10-10" @default.
• W1997883951 title "Influence of the critically ill state on host-pathogen interactions within the intestine: Gut-derived sepsis redefined" @default.
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• W1997883951 doi "https://doi.org/10.1097/01.ccm.0000045576.55937.67" @default.
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