In many forms of liver diseases such as alcoholic or nonalcoholic liver disease, liver failure and inflammation are the result of a cascade of insults which result in hyper-activation of inflammatory pathways and liver injury (26, 27) . Velayudham and colleagues (26) have shown that there is an up-regulation of TLR4 receptors in liver granulomas and LPS induced liver injury. Pathogen-induced TLR4 activation also activates reac- tive oxygen species (ROS), which is a major source of acute hepatocyte injury and death in the liver. Up-regulation of peripheral blood monocyte expression of TLR4 also occurs in patients with chronic hepatitis C (38) . In addition, endogenous gut-derived bacterial LPS have also been implicated as important cofactors in the pathogenesis of liver injury.