it produces high blood ethanol levels and is a model of binge drinking [15]. Inflammatory processes and activation of innate immunity is established as a critical component of alcoholic liver disease [24], [25] and is also emerging as an important determinant of alcohol effects on brain and on alcohol consumption [14], [26], [27]. Thus, it was of interest to compare immune activation following injection of lipopolysaccharide (LPS), which increases alcohol consumption, to the alcohol treatments. Microarrays were used to profile gene expression in two tissues (PFC and liver) from each of the four groups (three alcohol treatments, one LPS treatment), followed by data analysis to determine changes in gene expression produced by each treatment, the overlap of changes between treatments, pathway analysis of the gene networks and cellular enrichment of the differentially expressed genes. These data show distinct changes in gene expression in PFC and liver as well as among the treatments, but also show overlap between several of the treatments (notably, CI and LPS) and provide signaling networks that may mediate some of the consequences of chronic alcohol exposure. Comparison of gene expression changes among these four treatments and with published data on other animal models and human alcoholics
