Lipopolysaccharide (LPS) is the major lipid constituent of the cell wall of gram-negative bacilli and is known to trigger the acute-phase immune response. Inflammatory processes are characterized by the release of pro-inflammatory cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α, anti-inflammatory cytokines like IL-10 and endogenous IL-1 receptor antagonist (IL-1ra) (Feghali and Wright, 1997). These cytokines not only control local inflammatory processes in peripheral tissues and mediate immune responses but also affect central nervous system activity. They coordinate physiological responses such as fever, activate the hypothalamic–pituitary–adrenal axis, and induce behavioral changes, such as decreased intake of food and water, social withdrawal, anhedonia, and disturbed sleep, which are adaptive responses collectively termed “sickness behavior” (Dantzer, 2001). Some aspects of the acute sickness behavior such as anorexia can be produced by doses of LPS as low as 0.05 mg/kg (Wisse et al., 2007), whereas we found that at least 1 mg/kg LPS was required for the persistent increase in alcohol consumption. In addition, we saw no correlation between initial weight loss produced by LPS and increased alcohol consumption, suggesting
