Inflammation is important in the progress of alcoholic liver disease with Kupffer cell being the master regulator (see for recent reviews [1, 2]). In alcoholics and in ethanol-treated animals plasma LPS levels increase; moreover steatosis and ethanol consumption bring to intrahepatic inflammation due to Kupffer cells deregulated release of inflammatory cytokine (especially TNF-α). Several possibilities have been proposed to explain the increase of plasma LPS induced by alcohol. Clinical and experimental studies demonstrated a bacterial outgrowth after ethanol administration [13]; however LPS diffuses from intestine at very low levels. The main mechanism involved appears to be an increased intestinal permeability. Numerous studies demonstrated that ethanol disrupts the functional and structural integrity of intestinal epithelial cells resulting in cellular hyperpermeability and gut leakiness [14–16]. Oxidative stress and toxic metabolites accumulation in intestine may explain the increased permeability. Acetaldehyde, produced by ethanol oxidation in intestine, disrupts intestinal epithelial tight junctions and increases paracellular permeability to endotoxins in Caco-2 cell monolayer [17]. Furthermore, ethanol induces, in vitro and in vivo, the overproduction of nitric oxide, mediated by the inducible nitric oxide synthase [18, 19] that causes intestinal barrier dysfunction trough oxidation and nitration of cytoskeletal proteins [20].
