The causative agent of alcoholic liver disease is self-evident although the pathogenesis of the liver damage is not well understood. There is increasing evidence from both animal experiments and human studies that inflammation triggered in response to alcohol or its metabolites is important in the tissue damage and fibrosis of alcoholic liver disease. Both alcoholic hepatitis and alcoholic cirrhosis are characterized by inflammation of the liver, although the nature of the inflammatory infiltrate differs between the two diseases. The activation of leucocytes, their migration into tissue and subsequent interaction with target cells are all dependent on regulated adhesion. Therefore, leucocyte adhesion molecules and their counter-receptors will play a crucial role in determining the nature and activity of leucocytes infiltrating the liver in alcoholic liver disease. Evidence is now emerging that suggests roles for particular adhesion pathways in two aspects of the inflammatory response in alcoholic liver disease, (1) leucocyte recruitment to the liver, and (2) cell-mediated hepatocyte damage. It is important that these pathways are defined since therapy aimed at blocking leucocyte adhesion molecules might provide an effective future therapy for selected patients with alcoholic liver disease.