不少饮酒过度的人都有抗病能力变弱的感觉。英国学术刊物日前发表的一项新研究成果显示，长期摄入大量酒精会从两方面影响免疫力：使体内某些抗病毒物质含量下降；一些易引起发炎的物质含量随之上升。
新一期英国《ＢＭＣ免疫学》杂志刊登的报告说，美国马萨诸塞大学医学院的研究人员进行了相关实验。他们从一些健康志愿者体内提取组织样本，然后用酒精进行处理，其效果大概相当于一个人每天摄入６０克酒精且持续一个星期。
研究结果显示，在组织样本中，一些与免疫力有关的物质含量随之发生变化，其中有助于抵抗病毒感染的干扰素（ＩＦＮ）含量下降，而另一种名为“α型肿瘤坏死因子”（ＴＮＦ α）的促炎症物质含量会增多。
参加该研究的真吉·绍博教授说，酒精通过这两方面作用削弱人体免疫力，长期过度饮酒就会导致对许多疾病的抵抗力下降，如抵抗丙型肝炎病毒感染的能力会降低。因此为了保持身体健康，喜欢饮酒者应注意适度饮酒。
相关英文论文摘要：
Inhibition of TLR8- and TLR4-induced Type I IFN induction by alcohol is different from its effects on inflammatory cytokine production in monocytes
Background
Prolonged alcohol consumption is a significant co-factor in the progression of chronic viral infections including hepatitis C and HIV, which are both single-stranded RNA viruses. Toll like receptor 8 (TLR8), a pattern recognition receptor expressed in monocytes, senses viral single stranded RNA as a danger signal and leads to the induction of Type I interferon (IFN) as well as the pro-inflammatory cytokine, tumor necrosis factor alpha (TNF alpha). Lipopolysaccharide (LPS), a Toll like receptor 4 (TLR4) ligand, was shown to affect inflammatory cell activation after alcohol consumption and in HIV and HCV infections. Here we hypothesized that alcohol exposure modulates TLR8- and TLR4-ligand-induced monocyte activation and affects both type I IFN and inflammatory cytokine induction.
Results
The TLR8 ligand, CL075, as well as the TLR4 ligand, LPS, resulted in a significant induction of TNF alpha both at the mRNA and protein levels in human monocytes. We found that both acute and prolonged alcohol treatment resulted in inhibition of type I IFN induction by either TLR8 or TLR4 ligands in human monocytes at the protein and mRNA levels. In contrast to Type I IFN production, the effects of acute and prolonged alcohol were different on inflammatory cytokine activation after TLR8 or TLR4 ligand stimulation. Acute alcohol inhibited TLR8- or TLR4-induced TNF alpha protein and mRNA induction while it augmented IL-10 production in monocytes. In contrast, prolonged alcohol treatment augmented TNF alpha without affecting IL-10 production significantly in response to either TLR8 or TLR4 ligand stimulation.
Conclusions
These novel results suggest first, that alcohol has a profound inhibitory effect on Type I IFN induction regardless of intracellular (TLR8) or cell surface-derived (TLR4) danger signals. Second, both acute and prolonged alcohol exposure can inhibit antiviral Type I IFN pathway activation. Third, the opposite effects of acute (inhibitory) and prolonged alcohol (augmentation) treatment on pro-inflammatory cytokine activation extend to TLR8-induced signals beyond the previously shown TLR4/LPS pathway.
英文论文链接地址：https://www.biomedcentral.com/1471-2172/12/55/abstract
