Patel Jayshil J, Barash Mark
Division of Pulmonary, Critical Care, and Sleep Medicine, Medical College of Wisconsin, 8701 West Watertown Plank Road, 8th Floor: HUB for Collaborative Medicine, Milwaukee, WI, 53226, USA.
Curr Gastroenterol Rep. 2025 Dec;27(1):11. doi: 10.1007/s11894-024-00954-4. Epub 2025 Jan 10.
The purpose of this narrative review is to describe the mechanisms for gut dysfunction during critical illness, outline hypotheses of gut-derived inflammation, and identify nutrition and non-nutritional therapies that have direct and indirect effects on preserving both epithelial barrier function and gut microbiota during critical illness.
Clinical and animal model studies have demonstrated that critical illness pathophysiology and interventions breach epithelial barrier function and convert a normally commensal gut microbiome into a pathobiome. As a result, the gut has been postulated to be the "motor" of critical illness and numerous hypotheses have been put forward to explain how it contributes to systemic inflammation and drives multiple organ failure. Strategies to ameliorate gut dysfunction have focused on maintaining gut barrier function and promoting gut microbiota commensalism. The trajectory of critical illness may be closely related to gut epithelial barrier function, the gut microbiome and interventions that may contribute towards a deleterious pathobiome with immune dysregulation.
本叙述性综述旨在描述危重症期间肠道功能障碍的机制,概述肠道源性炎症的假说,并确定在危重症期间对维持上皮屏障功能和肠道微生物群具有直接和间接影响的营养及非营养疗法。
临床和动物模型研究表明,危重症的病理生理学及干预措施会破坏上皮屏障功能,并将正常共生的肠道微生物群转变为致病微生物群。因此,肠道被认为是危重症的 “驱动因素”,并且已经提出了许多假说来解释其如何导致全身炎症并引发多器官功能衰竭。改善肠道功能障碍的策略主要集中在维持肠道屏障功能和促进肠道微生物群共生关系上。危重症的发展轨迹可能与肠道上皮屏障功能、肠道微生物群以及可能导致具有免疫失调的有害致病微生物群的干预措施密切相关。