Figure 1.

In chronic liver diseases, dysbiosis and increased bacterial overgrowth provoke altered bile acid composition associated with reduced intestinal motility and the expression of tight junction proteins produces leaky gut. This leads to the increased passage of PAMPs, LPS, and bacterial products to the liver through the portal vein, with the consequent activation of inflammatory pathways. All of these alterations lead to increased ammonia production with consequent hepatic encephalopathy; the translocation of bacteria into the peritoneal fluid leading to spontaneous bacterial peritonitis; and the activation of proinflammatory and fibrotic pathways with increased hepatic vascular tone leading to portal hypertension.