Published online Nov 28, 2014. doi: 10.3748/wjg.v20.i44.16639
Revised: June 4, 2014
Accepted: July 11, 2014
Published online: November 28, 2014
Processing time: 280 Days and 6.3 Hours
Alcoholic liver disease (ALD) is the commonest cause of cirrhosis in many Western countries and it has a high rate of morbidity and mortality. The pathogenesis is characterized by complex interactions between metabolic intermediates of alcohol. Bacterial intestinal flora is itself responsible for production of endogenous ethanol through the fermentation of carbohydrates. The intestinal metabolism of alcohol produces a high concentration of toxic acetaldehyde that modifies gut permeability and microbiota equilibrium. Furthermore it causes direct hepatocyte damage. In patients who consume alcohol over a long period, there is a modification of gut microbiota and, in particular, an increment of Gram negative bacteria. This causes endotoxemia and hyperactivation of the immune system. Endotoxin is a constituent of Gram negative bacteria cell walls. Two types of receptors, cluster of differentiation 14 and Toll-like receptors-4, present on Kupffer cells, recognize endotoxins. Several studies have demonstrated the importance of gut-liver axis and new treatments have been studied in recent years to reduce progression of ALD modifying gut microbiota. It has focused attention on antibiotics, prebiotics, probiotics and synbiotics.
Core tip: A close anatomical and functional relationship between gut and liver exists. Blood circulated in the portal vein transfers various toxic compounds for filtration by liver. Endotoxin is a lipopolysaccharide derived from the cell wall of Gram negative bacteria presents in the intestine, which is absorbed from intestinal epithelium and transported to the liver and Kupffer cells through the portal vein. A qualitative (dysbiosis) and quantitative (bacterial overgrowth) alteration of intestinal microbiome are the causes of an increase of endotoxins and subsequently, liver damage. The new treatments try to contrast dysbiosis and bacterial overgrowth decreasing evolution of alcohol liver disease.