Iowa City VA Medical Center, Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, USA.
Alcohol Clin Exp Res. 2012 May;36(5):826-34. doi: 10.1111/j.1530-0277.2011.01678.x. Epub 2011 Dec 7.
Chronic ethanol (EtOH) consumption is associated with a wide variety of immune abnormalities including changes in T cells, B cells, dendritic cells, and natural killer (NK) cells. However, there is conflicting information as to the direction of such immune changes. The hypothesis that was tested in this report is that, for NK cells, the changes can vary as a function of the duration of alcohol ingestion.
Using the Meadows-Cook murine model of chronic alcohol ingestion, the changes in NK cell function and subset distribution were examined as a function of the duration of alcohol ingestion.
Acute alcohol ingestion resulted in decreased number and cytotoxic function of NK cells with no effect on intracellular interferon gamma expression. These abnormalities normalized after 12 to 14 days of alcohol ingestion and there was an increase of NK cell number and cytotoxicity after 8 weeks of continued EtOH ingestion. Ten weeks of continued alcohol consumption results in a significant decrease in the Ly49H+ CD11b+ CD27- splenic NK cell subset; this difference continued to be significant at 30 weeks.
This report may explain some of the conflicting data in the literature that examined NK cell activity in alcoholic patients. It is apparent that various abnormalities can be seen in NK cell activity and subset distribution with the flux being a function of the duration of alcohol ingestion. The demonstration of a decrease in the Ly49H+ subset (which is known to be involved in resisting murine cytomegalovirus infection) may explain the reported increase in susceptibility to some viral infections in chronic alcohol abuse. Another novel finding is that changes of some subsets of NK cells are not evident until at least 10 weeks of continued EtOH consumption.
慢性乙醇（EtOH）摄入与各种免疫异常有关，包括 T 细胞、B 细胞、树突状细胞和自然杀伤（NK）细胞的变化。然而，关于这些免疫变化的方向存在相互矛盾的信息。本报告测试的假设是，对于 NK 细胞，变化可以作为饮酒时间的函数而有所不同。
使用 Meadows-Cook 慢性酒精摄入的小鼠模型，检查 NK 细胞功能和亚群分布的变化作为酒精摄入时间的函数。
急性酒精摄入导致 NK 细胞数量和细胞毒性功能下降，而对细胞内干扰素γ表达没有影响。这些异常在酒精摄入 12 至 14 天后恢复正常，并且在继续摄入 EtOH 8 周后 NK 细胞数量和细胞毒性增加。持续饮酒 10 周导致脾脏 NK 细胞 Ly49H+ CD11b+ CD27-亚群数量显著减少；这种差异在 30 周时仍持续显著。
本报告可能解释了文献中检查酒精性患者 NK 细胞活性的一些相互矛盾的数据。显然，NK 细胞活性和亚群分布中可以看到各种异常，而这种异常是饮酒时间的函数。Ly49H+亚群数量减少（已知其参与抵抗鼠巨细胞病毒感染）的证明可能解释了慢性酒精滥用中一些病毒感染易感性增加的报道。另一个新发现是，一些 NK 细胞亚群的变化直到至少持续 10 周的 EtOH 消耗后才明显。
