Innate immune signaling and gut-liver interactions in non-alcoholic fatty liver disease.
Innate immune signaling and gut-liver interactions in non-alcoholic fatty liver disease.
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DOI：
10.3978/j.issn.2304-3881.2014.12.04
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发表时间：
2014-12-01
影响因子：
8
通讯作者：
Trautwein, Christian
中科院分区：
文献类型：
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作者：
Bieghs, Veerle;Trautwein, Christian
非酒精性脂肪性肝病（NAFLD）是代谢综合征的肝脏表现，涵盖了从脂肪变性到炎症、纤维化、肝硬化和肝细胞癌（HCC）的疾病谱。肝脏中的先天免疫应答在NAFLD进展过程中起着重要作用。此外，肠道微生物平衡和细菌移位的变化可进一步影响疾病进展。肝脏中的免疫细胞通过细胞内或表面表达的模式识别受体（PRR）识别细胞损伤或病原体入侵，随后启动信号级联反应，在NAFLD进展期间触发促进炎症反应的因子的释放。因此，免疫系统细胞被激活并招募到肝脏中的机制以及这些细胞如何引起损伤和应激对于理解NAFLD期间的炎症反应非常重要。
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and covers a disease spectrum ranging from steatosis to inflammation, fibrosis, cirrhosis and hepatocellular carcinoma (HCC). The innate immune response in the liver plays an important role during NAFLD progression. In addition, changes in the intestinal microbial balance and bacterial translocation can further affect disease progression. Immune cells in the liver recognize cell damage or pathogen invasion with intracellular or surface-expressed pattern recognition receptors (PRRs), subsequently initiating signaling cascades that trigger the release of factors promoting the inflammatory response during NAFLD progression. Therefore, mechanisms by which cells of the immune system are activated and recruited into the liver and how these cells cause injury and stress are important for understanding the inflammatory response during NAFLD.