Alcohol (ethanol) is a common dietary constituent that impacts heath. Heavy binge drinking increases mortality by escalating the risk of multisystem diseases in peripheral organs as well as psychiatric and neurological disorders in the central nervous system (CNS) [24]. Heavy alcohol drinkers have elevated levels of C-reactive protein, an innate immune marker [18,23]. Previously, we reported that levels of MCP-1, markers of microglia and NOX gp91phox were significantly increased in human postmortem alcoholic brain, compared to human moderate drinking control brain [25,26]. Further, we found that human postmortem alcoholic brain has increased histochemical markers of neuronal cell death [26]. Alcoholism is known to cause neurodegeneration [9]. We found that chronic administration of ethanol to mice increased brain and liver cytokines and chemokines, including TNFα, IL-1β and MCP-1 [27]. Although acute ethanol has been found to inhibit proinflammatory TLR responses, including the TLR3 agonist poly I:C [28,29], recent studies have found that toll-like receptors (TLRs) contribute to ethanol activation of brain proinflammatory responses and neurodegeneration [30]. These studies support a link among neuroinflammation, ethanol and systemic proinflammatory responses.
