The gut microbiome is recognized as a key factor in many liver diseases. Bacterial overgrowth is common in cirrhosis. Bacterial translocation is thought to cause spontaneous bacterial peritonitis. Lipopolysaccharide (LPS), a component of the gram negative bacterial cell wall, also translocates through permeable tight junctions of the gut, into the bloodstream. This is thought to be one possible trigger of splanchnic vasodilation in the hyperdynamic circulatory state of portal hypertension.
The gut microbiome is also implicated in pre-cirrhotic conditions. A great deal of this lecture described the pathogenic changes of alcohol use and the gut. We already know that alcohol acts directly on the liver; what is now recognized is the indirect effect on the liver through the gut-liver axis.
Studies involving rodents as well as humans show that when alcohol is consumed, the gut’s tight junctions become more permeable, and increased levels of circulating LPS and endotoxins can be measured in peripheral blood. All of the main cells in the liver express toll-like receptor 4 (TLR-4), the receptor for LPS. The liver thus recognizes the increased load of LPS and this activates an inflammatory cascade. This, of course, worsens any existing liver disease.
For more information on the fascinating relationship of the gut and liver, click on the link below: