Deletion of tumor progression locus 2 attenuates alcohol-induced hepatic inflammation

Excess consumption of alcohol is widespread throughout the world and chronic intoxication of alcohol is known to cause serious organ damage. The Center for Disease Control reports that as of 2011, over 50% of the United States population consumes alcohol (1). Of this population, 6.2%—almost 16 million individuals—are categorized with heavy alcohol use (defined as five or more drinks on the same occasion on each of 5 or more days in the past 30 days) and over 23% binge drink (defined as five or more drinks on the same occasion on at least 1 day in the past 30 days) (1). Specifically, alcohol consumption is one of the most prominent factors contributing to liver disease—a major cause of morbidity and mortality worldwide (2,3). The initial development of alcoholic liver disease (ALD) is characterized by hepatosteatosis (fatty liver) followed by the development of alcoholic steatohepatitis. The disease state can then further progress to the irreversible stages of fibrosis and cirrhosis, and increase the risk for hepatocellular carcinoma if alcohol consumption is continued (4-6)