Cellular and molecular mechanisms of alcoholic hepatitis: introduction and summary of the symposium

Abstract

The National Institute on Alcohol Abuse and Alcoholism and the Office of Rare Diseases, National Institutes of Health, sponsored a satellite symposium on “Cellular and Molecular Mechanisms of Alcoholic Hepatitis” at the 24th Annual Scientific Meeting of the Research Society on Alcoholism, Montreal, Quebec, Canada, June 2001. Alcohol intake is a major cause of hepatitis that may lead to alcoholic cirrhosis—a major cause of death in the United States. In up to one third of heavy drinkers alcoholic hepatitis develops, which is characterized by liver cell death and infiltration of leukocytes in hepatic parenchyma. Although leukocytes have been implicated in the pathogenesis of alcoholic hepatitis, the underlying cellular and molecular mechanisms by which leukocytes migrate to hepatic parenchyma and initiate tissue injury are not clear. For this symposium, 10 speakers were invited to address the following aspects of the mechanisms of alcoholic hepatitis: role of Kupffer cells in initiating the process of alcoholic hepatitis; types of leukocytes involved in the pathogenesis of alcoholic hepatitis; chemokines that are responsible for the attraction of leukocytes; adhesion molecules that promote the attachment of leukocytes to the endothelial cells and hepatocytes; mechanisms of leukocyte transmigration to hepatic parenchyma; mechanisms by which leukocytes initiate tissue injury; and interactive effects of alcohol and hepatitis viral proteins on liver injury. This article provides an introduction to the problem and a summary of the 10 scientific presentations delivered at the symposium.