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肠道微生物组和肠道屏障对肝脏疾病的贡献。

Contribution of the Intestinal Microbiome and Gut Barrier to Hepatic Disorders.

机构信息

Emory Vaccine Center, Division of Microbiology and Immunology, Yerkes National Primate Research Center, Emory University School of Medicine, Atlanta, Georgia.

Emory Vaccine Center, Division of Microbiology and Immunology, Yerkes National Primate Research Center, Emory University School of Medicine, Atlanta, Georgia; Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.

出版信息

Gastroenterology. 2020 Sep;159(3):849-863. doi: 10.1053/j.gastro.2020.04.077. Epub 2020 Jun 20.

Abstract

Intestinal barrier dysfunction and dysbiosis contribute to development of diseases in liver and other organs. Physical, immunologic, and microbiologic (bacterial, fungal, archaeal, viral, and protozoal) features of the intestine separate its nearly 100 trillion microbes from the rest of the human body. Failure of any aspect of this barrier can result in translocation of microbes into the blood and sustained inflammatory response that promote liver injury, fibrosis, cirrhosis, and oncogenic transformation. Alterations in intestinal microbial populations or their functions can also affect health. We review the mechanisms that regulate intestinal permeability and how changes in the intestinal microbiome contribute to development of acute and chronic liver diseases. We discuss individual components of the intestinal barrier and how these are disrupted during development of different liver diseases. Learning more about these processes will increase our understanding of the interactions among the liver, intestine, and its flora.

摘要

肠道屏障功能障碍和微生态失调导致肝脏和其他器官疾病的发生。肠道的物理、免疫和微生物学(细菌、真菌、古菌、病毒和原生动物)特征将其近 1000 万亿微生物与人体其他部位隔离开来。肠道屏障的任何一个方面出现故障,都可能导致微生物转移到血液中,并持续引发炎症反应,从而促进肝脏损伤、纤维化、肝硬化和致癌转化。肠道微生物种群或其功能的改变也会影响健康。我们回顾了调节肠道通透性的机制,以及肠道微生物组的变化如何导致急性和慢性肝病的发生。我们讨论了肠道屏障的各个组成部分,以及它们在不同肝病发展过程中是如何被破坏的。更多地了解这些过程将增加我们对肝脏、肠道及其菌群之间相互作用的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b27c/7502510/e3c892a121a0/nihms-1605456-f0001.jpg

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