A brief review of immunomodulation caused by acute administration of ethanol: involvement of neuroendocrine pathways.

Administration of EtOH to B6C3F1 mice by gavage produces blood EtOH levels, behavioral changes, and endocrine changes similar to those that have been reported in human binge drinkers. In the mouse model, EtOH causes thymic atrophy by a mechanism that seems to be predominantly glucocorticoid-dependent, although a synergistic role for other neuroendocrine mediators has not been ruled out. In contrast, the decreased numbers and activity of splenic NK cells in EtOH-treated mice does not seem to be caused by glucocorticoids, unless they act through type I glucocorticoid receptors (which are not antagonized by RU 486). Endogenous opioids also do not seem to be involved in this decrease in NK cell activity. A mechanism originating in the central nervous system is implicated by the observation that decreased NK cell activity can be prevented by the inverse agonist of the GABAA receptor, Ro15-4513. The neuroendocrine pathways leading to effects on NK cells, the proximate mediator(s) of these effects, and the biochemical changes in the NK cells that produce the effects are unknown.