The human intestine contains a diverse community of microbes that improve metabolism and

digestion in their symbiotic relationship with the host. However, alteration in its homeostasis can result in disease. The current study evaluated the factors that disrupt intestinal homeostasis and results in the development of non-alcoholic fatty liver disease (NAFLD), steatohepatitis (NASH), alcoholic liver disease, and cirrhosis.

It is evident that liver disease has long been related to qualitative and quantitative (overgrowth) dysbiotic changes in the intestinal microbiota. Various extrinsic factors, such as the Western diet and alcohol, can also effect these changes. Dysbiosis causes intestinal inflammation, a breakdown of the intestinal barrier, and translocation of microbial products in experimental models. Nevertheless, the involvement of the intestinal microbiome to liver disease goes beyond simple translocation of bacterial products that enhance hepatic injury and inflammation. Microbial metabolites produced in a dysbiotic intestinal environment and host factors are likewise significant in the pathogenesis of liver disease. The present study determined contribution of the combination of liver insult and disruptions in intestinal homeostasis in the liver disease.

More studies are required to determine microbial gene expression, proteins, and metabolites, and focus on patients with liver disease. Enhancing the knowledge of the delicate homeostasis between the intestine and its microbes could offer a new window into the pathogenesis of liver disease and treatment modalities. Evidences suggest a rationale attempt to modulate the intestinal microbiome to treat liver disease; however, the ultimate objective is to restore eubiosis, which in turn, could restore intestinal homeostasis.

Source: Schnabl B, Brenner DA. Interactions between the intestinal microbiome and liver diseases. Gastroenterology. 2014;146(6):1513-1524.