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Role of intestinal mucus and pancreatic proteases in the pathogenesis of trauma-hemorrhagic shock-induced gut barrier failure and multiple organ dysfunction syndrome

机译:肠粘液和胰蛋白酶在创伤性失血性休克诱导的肠屏障功能障碍和多器官功能障碍综合征发病机理中的作用

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摘要

The development of the multiple organ dysfunction syndrome (MODS) is one of the leading causes of death in critically ill patients. Owing to its clinical importance, MODS, as well as acute respiratory distress syndrome and systemic inflammatory response syndrome, has been the focus of significant research to delineate its causes as well as potential therapies for it. A large body of research has focused on the role of the gut in the pathogenesis of MODS, with a special focus on the mechanisms of gut injury as well as the processes by which a localized or limited gut injury is transduced into a systemic inflammatory state. Previous studies have focused on the systemic arm of gut ischemia-reperfusion injury and have largely ignored the non-bacterial intraluminal contents of the gut. The current review will present the hypothesis that the luminal contents of the gut, including the mucus gel layer and intraluminal pancreatic proteases as well as the gut flora, are critically involved in the pathogenesis of ischemia-reperfusion-induced gut injury and the subsequent development of gut-induced MODS.
机译:多器官功能障碍综合症(MODS)的发展是重症患者死亡的主要原因之一。由于其重要的临床意义,MODS以及急性呼吸窘迫综合征和全身性炎症反应综合征一直是描述其病因和潜在治疗方法的重要研究重点。大量的研究集中在肠道在MODS的发病机理中的作用,特别集中在肠道损伤的机制以及将局部或有限的肠道损伤转导为全身性炎症状态的过程。先前的研究集中在肠道缺血-再灌注损伤的全身部位,并且很大程度上忽略了肠道的非细菌内腔内容物。本综述将提出以下假设:肠道的内腔内容物,包括粘液凝胶层和腔内胰腺蛋白酶以及肠道菌群,均与缺血再灌注诱导的肠道损伤的发病机理以及随后的肠内炎症发展密切相关。肠道诱发的MODS。

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