Department of Medicine, University of California San Diego, La Jolla, California.
Department of Medicine, University of California San Diego, La Jolla, California.
Gastroenterology. 2014 May;146(6):1513-24. doi: 10.1053/j.gastro.2014.01.020. Epub 2014 Jan 15.
The human intestine harbors a diverse community of microbes that promote metabolism and digestion in their symbiotic relationship with the host. Disturbance of its homeostasis can result in disease. We review factors that disrupt intestinal homeostasis and contribute to nonalcoholic fatty liver disease, steatohepatitis, alcoholic liver disease, and cirrhosis. Liver disease has long been associated with qualitative and quantitative (overgrowth) dysbiotic changes in the intestinal microbiota. Extrinsic factors, such as the Western diet and alcohol, contribute to these changes. Dysbiosis results in intestinal inflammation, a breakdown of the intestinal barrier, and translocation of microbial products in animal models. However, the contribution of the intestinal microbiome to liver disease goes beyond simple translocation of bacterial products that promote hepatic injury and inflammation. Microbial metabolites produced in a dysbiotic intestinal environment and host factors are equally important in the pathogenesis of liver disease. We review how the combination of liver insult and disruptions in intestinal homeostasis contribute to liver disease.
人类肠道中栖息着多样化的微生物群落，它们与宿主共生，促进新陈代谢和消化。其体内平衡的破坏可导致疾病。我们综述了破坏肠道内环境稳态并导致非酒精性脂肪性肝病、脂肪性肝炎、酒精性肝病和肝硬化的因素。长期以来，肝脏疾病与肠道微生物群落的定性和定量（过度生长）失调变化相关联。外在因素，如西方饮食和酒精，促成了这些变化。肠道菌群失调导致肠道炎症、肠道屏障破坏和微生物产物易位。然而，肠道微生物组对肝脏疾病的影响不仅仅是简单的细菌产物易位，这些产物会促进肝损伤和炎症。在失调的肠道环境中产生的微生物代谢产物和宿主因素在肝脏疾病的发病机制中同样重要。我们综述了肝损伤和肠道内环境稳态破坏的共同作用如何导致肝脏疾病。
