Alverdy John C, Laughlin Robert S, Wu Licheng
Department of Surgery, University of Chicago Medical Center, IL 60637, USA.
Crit Care Med. 2003 Feb;31(2):598-607. doi: 10.1097/01.CCM.0000045576.55937.67.
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.
严重且持久的分解代谢应激状态已被证明对肠道微生物群和肠道功能有深远影响。肠源性脓毒症是一个术语，用于描述在严重分解代谢应激后出现全身炎症伴器官功能障碍的一种状态，据推测这种状态由肠道微生物群引发并持续存在。关于这一过程机制的普遍观点认为，应激促进肠道细菌或其毒素向全身循环转移，导致促炎细胞因子释放，这些细胞因子参与全身炎症反应综合征。本综述试图通过关注肠道内宿主 - 病原体相互作用所产生的分子事件来重新定义肠源性脓毒症的机制。这篇基于证据的综述指出，即使存在强效医院病原体，肠源性菌血症引发促炎的可能性也很低，其本身不足以引发全身炎症反应以及严重且持久的分解代谢应激后通常出现的器官衰竭状态。本文还讨论了这一明显矛盾现象的机制。
