Astrocytes express receptors necessary for neuroimmune activation, including cytokine and chemokine receptors and TLRs. TLR3, for example, is enriched in astrocytes and its expression increases in response to LPS (McCarthy et al., 2017a). Ethanol promotes TLR4 and IL-1R signaling in cultured astrocytes, causing increased expression of inflammatory cytokines (IL-1β, TNF-α, IL-6, iNOS, and COX-2) (Alfonso-Loeches et al., 2010; Blanco et al., 2004, 2005). GFAP up-regulation in ethanol-exposed rodents is likely regulated by TLR4 (Alfonso-Loeches et al., 2013) and PDE4B (Avila et al., 2017). Ethanol-induced cytokine release from astrocytes may be mediated by NLRP3 activation (Alfonso-Loeches et al., 2014). Current evidence also points to a role for astrocyte-specific immune signaling in alcohol-dependent behaviors. Astrocytes may contribute to ethanol-induced increases in the cytokine CCL2 in rodents (Kane et al., 2014). Transgenic mice over-expressing CCL2 in astrocytes have slightly reduced alcohol consumption (Bray et al., 2017). These mice also exhibit differences in the effect of ethanol exposure on synaptic protein levels in the hippocampus compared with non-transgenic littermate controls (Gruol et al., 2014). In hippocampal slices, astrocyte-specific increases in CCL2 or the inflammatory
