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首页> 外文期刊>Infection and immunity >A Low Concentration of Ethanol Reduces the Chemiluminescence of Human Granulocytes and Monocytes but Not the Tumor Necrosis Factor Alpha Production by Monocytes after Endotoxin Stimulation
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A Low Concentration of Ethanol Reduces the Chemiluminescence of Human Granulocytes and Monocytes but Not the Tumor Necrosis Factor Alpha Production by Monocytes after Endotoxin Stimulation

机译：低浓度的乙醇减少内毒素刺激后人粒细胞和单核细胞的化学发光，但不会降低单核细胞产生的肿瘤坏死因子α

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The ability of polymorphonuclear neutrophils (PMNs) and monocytes (Mφ) to produce reactive oxygen species (ROS) has been related closely to their potential in the killing of microorganisms. Ethanol has been shown to impair the generation of ROS in these phagocytes after stimulation with some immunogens and to increase the susceptibility of alcohol abusers to infectious diseases. As endotoxemia is common in alcohol abusers, we investigated the effect of ethanol (21.7 mmol/liter) on the luminol-amplified chemiluminescence of PMNs and Mφ after endotoxin stimulation and the release of tumor necrosis factor alpha (TNF-α) from Mφ. Further, the efficiency of ethanol to inactivate chemically generated ROS was tested. Significant stimulation of ROS release occurred at endotoxin concentrations of 1 ng/ml or higher in both PMNs and Mφ. Ethanol significantly suppressed the formation of ROS in both cell types, the decrease being more pronounced in Mφ (?73.8%) than in PMNs (?45.7%). The correlations between endotoxin concentration and the amount of released ROS showed a dose-dependent, sigmoidal course. Concentrations of endotoxin necessary for half-maximum stimulation were nearly identical (6 to 8 ng/ml) in both PMNs and Mφ, independent of the presence of ethanol. In contrast to ROS formation, ethanol had no effect on the amount of TNF-α produced by endotoxin-stimulated Mφ. Ethanol was shown to be unable to decrease the levels of chemically generated ROS under physiological conditions. Therefore, ethanol cannot be assumed to be an “antioxidative” compound but rather seems to modify processes of endotoxin recognition, intracellular signal transduction, or metabolism.
机译：多形核中性粒细胞（PMNs）和单核细胞（Mφ）产生活性氧（ROS）的能力与它们杀死微生物的潜力密切相关。业已证明，乙醇会在受到某些免疫原刺激后削弱这些吞噬细胞中ROS的生成，并增加酗酒者对传染病的敏感性。由于内毒素血症在酗酒者中很常见，因此我们研究了乙醇（21.7 mmol / L）对内毒素刺激后Luminol增强的PMN和Mφ化学发光以及从Mφ中释放肿瘤坏死因子α（TNF-α）的影响。此外，测试了乙醇灭活化学生成的ROS的效率。在PMN和Mφ中，当内毒素浓度为1 ng / ml或更高时，ROS释放受到明显刺激。乙醇可显着抑制两种细胞类型中ROS的形成，Mφ（？73.8％）比PMNs（？45.7％）更明显。内毒素浓度与释放的ROS量之间的相关性显示出剂量依赖性的S形过程。在PMN和Mφ中，半最大刺激所需的内毒素浓度几乎相同（6至8 ng / ml），与乙醇的存在无关。与ROS形成相反，乙醇对内毒素刺激的Mφ产生的TNF-α的量没有影响。乙醇在生理条件下不能降低化学生成的ROS的水平。因此，乙醇不能被认为是一种“抗氧化”化合物，而是似乎会改变内毒素识别，细胞内信号转导或新陈代谢的过程。

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