of both innate and adaptive immunity (Boersma and Meffert, 2008), and NF-κB and its signaling pathways have become a focal point for intense drug discovery efforts (Gupta et al., 2010; Karin et al., 2004). NF-κB is a point of convergence for many extracellular signals that activate gene expression and plays a key role in inflammation and disease (Gamble et al., 2012; Schmid and Birbach, 2008). Considering evidence for the neuroimmune system in regulating ethanol drinking (Harris and Blednov, 2013; Mayfield et al., 2013) and the role of PPARs in reducing inflammation, PPAR agonists may reduce drinking via their anti-inflammatory mechanisms. This might be expected if the drinking models used here induce sufficient immune activation. Altered expression of immune-related genes was observed in liver and prefrontal cortex from C57BL/6J mice after chronic ethanol treatment (Osterndorff-Kahanek et al., 2013). Changes were greatest in liver compared to prefrontal cortex and differed depending on the ethanol treatment paradigm. Systemic injection of PPAR agonists also induced changes in the expression of immune-related genes in the liver but did not produce prominent changes in neuroimmune pathways in C57BL/6J mice (Ferguson et al., 2014). NF-κB targets were not downregulated in liver or brain following PPAR agonist treatment,
