Interactions Between the Intestinal Microbiome and Liver Diseases

By B. Schnabl, D. Brenner. Gastroenterology, 2014

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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 non-alcoholic fatty liver disease (NAFLD), steatohepatitis (NASH), 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.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/bd6465e3416614b1e50d6e3c05701b1260bcab98

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Citations in the corpus

Hepatic fibrosis: Concept to treatment. (2015, background): “Other major areas of development include the role of intestinal microbiota [15,16], the role of tissue hypoxia [17] with the establishment of an anaerobic pro-inflammatory environment [18], the influence of epigenetic modification in conditioning the progression of fibrosis [19] and the weight of ti”
Liver inflammation and fibrosis. (2017, background): “Necroptosis, as defined by RIP3-dependent mixedlineage kinase domain-like protein activation, is triggered in the liver of mouse models of NASH and in human NAFLD, whereas absence of RIP3 ameliorates liver injury, steatosis, inflammation, and fibrosis in an experimental NASH model (17).”
The severity of NAFLD is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota (2016, background): “Recent animal studies have placed the gut microbiota as a potentially important player in the pathogenesis of NAFLD.((14,15)) However, data linking gut dysbiosis with the severity of NAFLD remain poorly documented in humans.”
Hepatic Inflammation and Fibrosis: Functional Links and Key Pathways (2015, background): “Multiple mechanisms have been suggested to promote the progression from simple steatosis to NASH and NASH-associated fibrosis: (1) inflammatory cytokines released from “inflamed adipose tissues” in obese patients(99); (2) ROS production by dysregulated hepatic lipid and cholesterol metabolism(99); a”