Mechanisms of alcohol-mediated hepatotoxicity in human-immunodeficiency-virus-infected patients

Figure 2 Alcohol-induced hepatocyte damage is amplified by human immunodeficiency virus infection. The current model of alcohol-induced liver disease includes increased gut-derived lipopolysaccharide (LPS) entry into the liver where Kupffer cells are activated via LPS/Toll-like receptor (TLR) 4 and produce tumor necrosis factor (TNF)α. Human immunodeficiency virus (HIV) infection also increases gut-derived LPS levels in the circulating blood. Increased production of TNFα will act on alcohol-exposed hepatocytes to induce apoptosis. ROS: Reactive oxygen species.