Wu W J, Pruett S B
Department of Biological Sciences, Mississippi State University, Mississippi, USA.
Alcohol Clin Exp Res. 1997 Sep;21(6):1030-6.
Ethanol (EtOH) suppresses splenic natural killer (NK) cell activity in a mouse binge drinking model. Direct effects of EtOH and its metabolites are not the major cause of this suppression. Also, catecholamines do not completely explain this suppression. This implicates the involvement of other neuroendocrine mediators in this suppression. Previous studies in this laboratory have shown that RU 486 at a dosage of 100 mg/kg did not affect EtOH-induced suppression of NK cell activity. However, in the present study, RU 486 at a dosage of 200 mg/kg partially blocked the suppression of NK cell activity induced by EtOH. Moreover, corticosterone at levels expected in the free (unbound) form in EtOH-treated mice decreased NK cell activity in vitro. Nadolol in combination with RU 486 blocked the suppression of NK cell activity in EtOH-treated mice. Although there were reasons to suspect that EtOH-induced changes in the levels of growth hormone or prolactin might also contribute to the suppression of NK cell activity; evidence obtained herein did not indicate such involvement. Thus, glucocorticoids and catecholamines seem to be involved in EtOH-induced suppression of NK cell activity. Together, with the direct effects of EtOH, these neuroendocrine mediators seem to be sufficient to explain all of the suppression of NK cell activity caused by EtOH.
在小鼠暴饮模型中，乙醇（EtOH）会抑制脾脏自然杀伤（NK）细胞的活性。乙醇及其代谢产物的直接作用并非这种抑制作用的主要原因。此外，儿茶酚胺也不能完全解释这种抑制作用。这意味着其他神经内分泌介质参与了这种抑制作用。本实验室之前的研究表明，100mg/kg剂量的RU 486不会影响乙醇诱导的NK细胞活性抑制。然而，在本研究中，200mg/kg剂量的RU 486部分阻断了乙醇诱导的NK细胞活性抑制。此外，乙醇处理小鼠体内游离（未结合）形式的皮质酮水平降低了体外NK细胞的活性。纳多洛尔与RU 486联合使用可阻断乙醇处理小鼠的NK细胞活性抑制。尽管有理由怀疑乙醇诱导的生长激素或催乳素水平变化也可能导致NK细胞活性抑制；但本文获得的证据并未表明存在这种关联。因此，糖皮质激素和儿茶酚胺似乎参与了乙醇诱导的NK细胞活性抑制。这些神经内分泌介质与乙醇的直接作用一起，似乎足以解释乙醇引起的NK细胞活性的所有抑制作用。
