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本文引用的文献

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J Intensive Care. 2019 Mar 20;7:17. doi: 10.1186/s40560-019-0372-6. eCollection 2019.
2
Gut rest strategy and trophic feeding in the acute phase of critical illness with acute gastrointestinal injury.危重症伴有急性胃肠损伤患者的急性期中的肠道休息策略和营养性喂养。
Nutr Res Rev. 2019 Dec;32(2):176-182. doi: 10.1017/S0954422419000027. Epub 2019 Mar 28.
3
Goblet cells: multifaceted players in immunity at mucosal surfaces.杯状细胞:黏膜表面免疫中的多面手。
Mucosal Immunol. 2018 Nov;11(6):1551-1557. doi: 10.1038/s41385-018-0039-y. Epub 2018 Jun 4.
4
The Intestinal Epithelium: Central Coordinator of Mucosal Immunity.肠上皮:黏膜免疫的中枢协调者。
Trends Immunol. 2018 Sep;39(9):677-696. doi: 10.1016/j.it.2018.04.002. Epub 2018 Apr 30.
5
Chronic Alcohol Ingestion Worsens Survival and Alters Gut Epithelial Apoptosis and CD8+ T Cell Function After Pseudomonas Aeruginosa Pneumonia-Induced Sepsis.慢性酒精摄入可降低铜绿假单胞菌肺炎致脓毒症后生存率,并改变肠道上皮细胞凋亡和 CD8+T 细胞功能。
Shock. 2019 Apr;51(4):453-463. doi: 10.1097/SHK.0000000000001163.
6
Regulators of Intestinal Epithelial Migration in Sepsis.脓毒症中肠道上皮细胞迁移的调控。
Shock. 2019 Jan;51(1):88-96. doi: 10.1097/SHK.0000000000001117.
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Probiotics for Preventing Ventilator-Associated Pneumonia in Mechanically Ventilated Patients: A Meta-Analysis with Trial Sequential Analysis.益生菌预防机械通气患者呼吸机相关性肺炎:一项采用序贯试验分析的Meta分析
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8
Gut microbiota and host defense in critical illness.肠道微生物群与危重病中的宿主防御
Curr Opin Crit Care. 2017 Aug;23(4):257-263. doi: 10.1097/MCC.0000000000000424.
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Collapse of the Microbiome, Emergence of the Pathobiome, and the Immunopathology of Sepsis.微生物群的崩溃、致病生物群的出现与脓毒症的免疫病理学
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危重症中肠道损伤的病理生理学及保护措施

Pathophysiology and protective approaches of gut injury in critical illness.

作者信息

Jung Chang Yeon, Bae Jung Min

机构信息

Department of Surgery, Yeungnam University Hospital, Daegu, Korea.

Department of Surgery, Yeungnam University College of Medicine, Daegu, Korea.

出版信息

Yeungnam Univ J Med. 2021 Jan;38(1):27-33. doi: 10.12701/yujm.2020.00703. Epub 2020 Sep 23.

DOI:10.12701/yujm.2020.00703
PMID:33022904
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7787898/
Abstract

The gut is a complex organ that has played an important role in digestion, absorption, endocrine functions, and immunity. The gut mucosal barriers consist of the immunologic barrier and nonimmunologic barrier. During critical illnesses, the gut is susceptible to injury due to the induction of intestinal hyperpermeability. Gut hyperpermeability and barrier dysfunction may lead to systemic inflammatory response syndrome. Additionally, gut microbiota are altered during critical illnesses. The etiology of such microbiome alterations in critical illnesses is multifactorial. The interaction or systemic host defense modulation between distant organs and the gut microbiome is increasingly studied in disease research. No treatment modality exists to significantly enhance the gut epithelial integrity, permeability, or mucus layer in critically ill patients. However, multiple helpful approaches including clinical and preclinical strategies exist. Enteral nutrition is associated with an increased mucosal barrier in animal and human studies. The trophic effects of enteral nutrition might help to maintain the intestinal physiology, prevent atrophy of gut villi, reduce intestinal permeability, and protect against ischemia-reperfusion injury. The microbiome approach such as the use of probiotics, fecal microbial transplantation, and selective decontamination of the digestive tract has been suggested. However, its evidence does not have a high quality. To promote rapid hypertrophy of the small bowel, various factors have been reported, including the epidermal growth factor, membrane permeant inhibitor of myosin light chain kinase, mucus surrogate, pharmacologic vagus nerve agonist, immune-enhancing diet, and glucagon-like peptide-2 as preclinical strategies. However, the evidence remains unclear.

摘要

肠道是一个复杂的器官,在消化、吸收、内分泌功能和免疫方面发挥着重要作用。肠道黏膜屏障由免疫屏障和非免疫屏障组成。在危重病期间,由于肠道通透性增加,肠道易受损伤。肠道通透性增加和屏障功能障碍可能导致全身炎症反应综合征。此外,危重病期间肠道微生物群会发生改变。危重病中这种微生物群改变的病因是多因素的。在疾病研究中越来越多地研究远处器官与肠道微生物群之间的相互作用或全身宿主防御调节。目前尚无治疗方法能显著增强危重病患者的肠道上皮完整性、通透性或黏液层。然而,存在多种有益的方法,包括临床和临床前策略。在动物和人体研究中,肠内营养与黏膜屏障增加有关。肠内营养的营养作用可能有助于维持肠道生理功能、防止肠绒毛萎缩、降低肠道通透性并预防缺血再灌注损伤。有人提出了微生物群方法,如使用益生菌、粪便微生物移植和消化道选择性去污。然而,其证据质量不高。为促进小肠快速肥大,已报道了多种因素,包括表皮生长因子、肌球蛋白轻链激酶的膜渗透抑制剂、黏液替代物、药理学迷走神经激动剂、免疫增强饮食和胰高血糖素样肽-2作为临床前策略。然而,证据仍不明确。