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首页> 外文期刊>Life sciences >Acute ethanol administration profoundly alters poly I:C-induced cytokine expression in mice by a mechanism that is not dependent on corticosterone.
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Acute ethanol administration profoundly alters poly I:C-induced cytokine expression in mice by a mechanism that is not dependent on corticosterone.

机译：急性乙醇管理通过一种不依赖皮质酮的机制，深刻改变了多聚I：C诱导的小鼠细胞因子的表达。

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摘要

Polyinosinic polycytidylic acid (poly I:C) is an analog of double stranded RNA, which is a common replication intermediate for many viruses. It acts through a toll-like receptor (TLR3) to induce a group of cytokines that can mediate host resistance to viruses and some cancers. The effect of ethanol (EtOH) on induction of this set of cytokines has not been determined. Mice were treated with a single dose of EtOH (by gavage) at the same time as poly I:C was administered (intraperitoneally), and cytokine mRNA expression was measured by RNAse protection assay. Concentrations of IFN-alpha, IL-10, and IL-12 in the serum were measured by ELISA. A single dose of EtOH suppressed induction of mRNA for IFN-alpha, IFN-beta, IFN-gamma, IL-6, IL-9, IL-12, and IL-15. The concentrations of IFN-alpha and IL-12 in the serum were also decreased. In contrast, IL-10 was minimally induced by poly I:C alone, but it was substantially induced by poly I:C plus EtOH. Dose response and time course studies demonstrated that significant alterations of IFN-alpha, IL-10, and IL-12 expression occurred at dosages as low as 4 g/kg (a dosage previously shown to produce blood EtOH concentrations of approximately 0.2%) and that alterations persisted at least 4-6 hr after administration of EtOH. The glucocorticoid synthesis inhibitor, aminoglutethimide, diminished corticosterone levels to normal, but did not block the effects of EtOH on cytokine expression. These results demonstrate that EtOH affects the expression of poly I:C-induced cytokines and that this action is not mediated by corticosterone. These results plus previously published findings are consistent with the idea that EtOH may be a generalized suppressor of toll-like receptor signaling.
机译：聚肌苷酸聚胞苷酸（poly I：C）是双链RNA的类似物，双链RNA是许多病毒的常见复制中间体。它通过通行费样受体（TLR3）起作用，诱导一组细胞因子，这些细胞因子可以介导宿主对病毒和某些癌症的抵抗力。尚未确定乙醇（EtOH）对这组细胞因子的诱导作用。在施用聚I：C（腹膜内）的同时，用单剂量的EtOH（通过管饲法）治疗小鼠，并通过RNA酶保护测定法测量细胞因子mRNA的表达。通过ELISA测量血清中IFN-α，IL-10和IL-12的浓度。单剂量EtOH可抑制IFN-α，IFN-β，IFN-γ，IL-6，IL-9，IL-12和IL-15的mRNA诱导。血清中IFN-α和IL-12的浓度也降低。相比之下，IL-10仅由poly I：C诱导最小，但基本上由poly I：C加EtOH诱导。剂量反应和时程研究表明，低至4 g / kg的剂量（先前显示的剂量产生的血液EtOH浓度约为0.2％）会显着改变IFN-α，IL-10和IL-12的表达，在施用EtOH后至少4-6小时内这种变化持续存在。糖皮质激素合成抑制剂氨基谷氨酰胺使皮质酮水平降低至正常水平，但并未阻止EtOH对细胞因子表达的影响。这些结果表明，EtOH影响多聚I：C诱导的细胞因子的表达，并且该作用不是由皮质酮介导的。这些结果加上先前发表的发现与EtOH可能是toll样受体信号转导的普遍抑制因素的想法相一致。

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