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Bacterial and eukaryotic extracellular vesicles and non-alcoholic fatty liver disease: new players in the gut-liver axis?
American Journal of Physiology-Gastrointestinal and Liver Physiology ( IF 3.9 ) Pub Date : 2021-01-20 , DOI: 10.1152/ajpgi.00362.2020
Alexandre Villard 1 , Jérôme Boursier 2 , Ramaroson Andriantsitohaina 3
Affiliation  

The liver and intestine communicate in a bi-directional way through the biliary tract, portal vein, and other components of the gut-liver axis. The gut microbiota is one of the major contributors to the production of several proteins and bile acids. Imbalance in the gut bacterial community, called dysbiosis, participates in the development and progression of several chronic liver diseases, such as non-alcoholic fatty liver disease (NAFLD). NAFLD is currently considered the main chronic liver disease worldwide. Dysbiosis contributes to NAFLD development and progression, notably by a greater translocation of pathogen-associated molecular patterns (PAMPs) in the blood. Lipopolysaccharide (LPS) is a PAMP that activates toll-like receptor 4 (TLR4), induces liver inflammation, and participates in the development of fibrogenesis. LPS can be transported by bacterial extracellular vesicles (EVs). EVs are spherical structures produced by eukaryotic and prokaryotic cells that transfer information to distant cells and may represent new players in NAFLD development and progression. The present review summarizes the role of eukaryotic EVs, either circulating or tissue-derived, in NAFLD features, such as liver inflammation, angiogenesis, and fibrosis. Circulating EV levels are dynamic and correlate with disease stage and severity. However, scarce information is available concerning the involvement of bacterial EVs in liver disease. The present review highlights a potential role of bacterial EVs in insulin resistance and liver inflammation, although the mechanism involved has not been elucidated. Additionally, because of their distinct signatures, eukaryotic and prokaryotic EVs may also represent a promising NAFLD diagnostic tool as a "liquid biopsy" in the future.

中文翻译:

细菌和真核细胞外囊泡和非酒精性脂肪肝:肠肝轴的新参与者?

肝和肠通过胆道,门静脉和肠肝轴的其他组件双向通信。肠道菌群是几种蛋白质和胆汁酸生产的主要贡献者之一。肠道细菌群落的失衡,被称为dysbiosis,参与了几种慢性肝病的发展和进程,例如非酒精性脂肪肝(NAFLD)。NAFLD目前被认为是世界范围内主要的慢性肝病。营养不良会促进NAFLD的发展和进程,特别是通过血液中病原体相关分子模式(PAMP)的更大移位。脂多糖(LPS)是一种PAMP,可激活Toll样受体4(TLR4),诱导肝炎症并参与纤维发生的发展。LPS可以通过细菌细胞外囊泡(EVs)转运。电动汽车是由真核和原核细胞产生的球形结构,它们将信息转移到远处的细胞,并可能代表着NAFLD发育和发展的新参与者。本综述总结了循环或组织来源的真核电动车在NAFLD功能(例如肝脏炎症,血管生成和纤维化)中的作用。循环EV水平是动态的,并且与疾病阶段和严重程度相关。但是,关于细菌电动车与肝脏疾病的关系的信息很少。本综述着重指出了细菌电动车在胰岛素抵抗和肝脏炎症中的潜在作用,尽管其机制尚不清楚。此外,由于其独特的签名,
更新日期:2021-01-21
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