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Minerva Gastroenterol Dietol. 2017 Dec;63(4):385-398. doi: 10.23736/S1121-421X.17.02375-3.

Gut microbiota and the liver.

Author information

1
Department of Clinical and Experimental Medicine, University of Campania "L. Vanvitelli", Naples, Italy - alessandro.federico@unina2.it.
2
Department of Clinical and Experimental Medicine, University of Campania "L. Vanvitelli", Naples, Italy.

Abstract

Nowadays liver diseases represent one of major healthy problems in the world in terms of morbidity and mortality. The high prevalence of liver pathologies represents the key point to understand the necessity to identify the pathogenetic mechanisms that support these disorders in order to nurse them. Alterations of intestinal microbiota seem to play an important role in induction and promotion of liver damage progression, in addition to direct injury resulting from different causal agents. Gut microbiota is considered both as a promoting factor and as a potential therapeutic target of a large number of liver pathologies due to the connection between intestine and liver: the gut-liver axis. This connection influences absorption and deposition of nutrients into the liver, but also induces the activation of toll-like receptors due to the passage of pathogen-associated molecular patterns in the portal blood and therefore may start both the development of liver damage and its consequent progression to more advanced stages, including cirrhosis and hepatocarcinoma. The gut liver axis also includes the intestinal permeability (IP) degree. It is very variable and interconnected to several factors, most of them dependent from gut microbiota, that is the "lead" in the control of IP. This revue is aimed to report the more recent knowledges about gut microbiota and chronic liver disease, from liver steatosis to cirrhosis and its complications, including hepatocellular carcinoma. For these reasons, it could be useful to intervene, through suitable therapeutic approaches, on the interruption of mechanisms that underlie dysbiosis, IP increase, activation of liver inflammasome, hepatic stellate cells and hepatocarcinogenic processes in order to reduce the liver damage.

PMID:
28927250
DOI:
10.23736/S1121-421X.17.02375-3
[Indexed for MEDLINE]

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