Microglial activation occurs in a variety of neurological conditions and diseases, and increasing number of studies show that microglial activation contributes to the neuroinflammation associated with chronic alcohol exposure and withdrawal. Studies indicate that innate immune signaling plays a role in alcohol addiction, and genes implicated in neuroinflammatory processes accompanying alcoholism are expressed in microglia [1–3]. Supporting a role for microglial activation are studies showing that treatment with minocycline, which selectively reduces microglia activation, reduces alcohol intake as well as acute actions of ethanol on sedation and motor impairment [4, 5], and similarly, treatment of mice with tigecycline, another tetracycline derivative, reduced alcohol consumption and clinical features of alcohol consumption in mice [6]. There are also increasing studies demonstrating that microglia can be directly activated by alcohol leading to increases in inflammatory factors including cytokines, chemokines, transcription factors, and their receptors [1, 2, 7–13]. In many cases, the effects of alcohol were shown to involve activation of the Tlr4 receptor [9, 10, 12, 14–17] which can directly activate inflammatory transcription factor NFkB and subsequently increase of inflammatory gene expression. Alcohol
