Acute ethanol intake attenuates inflammatory cytokines after brain injury in rats: a possible role for corticosterone. 
It has been reported that acute ethanol intoxication exerts dose-dependent effects, both beneficial and detrimental, on the outcome of traumatic brain injury (TBI), although the mechanism(s) has not been determined.  Given that pro-inflammatory cytokines are either neuroprotective or neurotoxic, depending on their tissue levels, ethanol-induced alterations in brain cytokine production may be involved in determining the recovery after TBI.  The present study was undertaken to examine the effect of acute ethanol pretreatments (producing blood alcohol concentrations of 100+/-16 mg/dL, and 220+/-10 mg/dL, considered low and intoxicating doses, respectively) on interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) levels in discrete brain regions.  In addition, serum corticosterone levels were also examined because the hormone is a modulator of cytokine production, its secretion is stimulated by ethanol, and it has been associated with the severity of post-injury neurologic dysfunction.  The data presented in this report demonstrate that moderate cortical impact brain injury elicits a marked increase in IL-1beta and TNF-alpha in the injured cortex as well as in the hippocampus ipsilateral to the injury.  Ethanol pretreatment lowered cytokine levels in the cortex, hippocampus and hypothalamus in a dose-dependent manner after TBI compared to the untreated injured rats.  Serum corticosterone levels were markedly increased in the injured rats, and were further augmented in the ethanol-pretreated injured animals in a dose-dependent manner.  Our findings suggest that ethanol-induced decrease in pro-inflammatory cytokine production may be linked to increased circulating corticosterone, both of which may contribute to the outcome of brain injury.