genomic changes in different animal models. One theme that has emerged from studies of gene expression in human alcoholism is the role of neuroimmune genes [3], [11], [12] and differential expression of this category of genes is also seen in mice with genetic predisposition for high alcohol consumption [13]. In addition, activation of the innate immune system with LPS and the availability of chronic ethanol both increase alcohol consumption [14], [15]. This raises the question of which, if any, of the rodent models of excessive alcohol consumption show changes in gene expression, neuroimmune genes, in particular, that might be similar to human alcoholism and similar to the immune activation produced by LPS. A major consequence of chronic alcohol consumption is altered liver function, often accompanied by steatosis and other alcoholic liver injuries. A few studies have examined changes in liver gene expression produced by administration of alcohol by chronic intragastric infusion or consumption of a liquid diet [16], [17], but there is a paucity of studies of liver gene expression profiles in any of the mouse models of voluntary alcohol consumption.
