The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host’s organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut–liver axis. The gut–liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut–brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood–brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut–liver axis and gut–brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.
The Purinergic P2X7 Receptor-NLRP3 Inflammasome Pathway: A New Target in Alcoholic Liver Disease?
