Microglia, the resident innate immune cells in the brain, produce proinflammatory factors that contribute to neurodegeneration through increased proinflammatory superoxide and other toxic agents [6]. In previous studies, we found that the postmortem human alcoholic brain showed increased Iba1 + IR, a microglial marker [25]. We investigated microglial Iba1 + IR to evaluate size and morphological changes of microglia. Control subjects showed resting microglial morphology (Figure 4), with mild increases in Iba1 + IR staining with ethanol or poly I:C alone treatment (images not shown). Ethanol pretreatment further potentiated poly I:C increased Iba1 + IR. Multiple brain regions, including cortex and dentate gyrus, showed increased Iba1 + IR (Figure 4). These studies indicate that ethanol primes microglia and potentiates TLR3 agonist poly I:C activation of microglia.
