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首页> 外文期刊>Infection and immunity >Enhancement of Lipopolysaccharide-Induced Neutrophil Oxygen Radical Production by Tumor Necrosis Factor Alpha
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Enhancement of Lipopolysaccharide-Induced Neutrophil Oxygen Radical Production by Tumor Necrosis Factor Alpha

机译：肿瘤坏死因子α增强脂多糖诱导的中性粒细胞氧自由基的产生。

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Although tissues become exposed to both exogenous and endogenous cell-activating mediators during infection, there is little appreciation of the effects of subjecting cells to multiple mediators. We examined the hypothesis that the response of neutrophils to bacterial lipopolysaccharide (LPS) is significantly altered in the presence of the endogenous mediator tumor necrosis factor alpha (TNF). The data showed that human neutrophils pretreated with TNF for 10 to 30 min, displayed significantly enhanced superoxide production in response to LPS (from eitherEscherichia coli K-235 or E. coli 0127:B8), measured as lucigenin-dependent chemiluminescence (CL), seen as an increase in the initial peak rate as well as the total CL accumulated over the incubation period. TNF amplified the response to LPS at 1 to 100 U of TNF/106 neutrophils and was able to enhance the response to a wide range of concentrations of LPS (0.01 to 1,000 ng/ml). The TNF-induced increase in the LPS response was paralleled by an increase in LPS binding to the neutrophils, which could be abrogated by an anti-CD14 monoclonal antibody. The results demonstrate that TNF significantly increases the LPS-induced release of oxygen radicals in neutrophils through the upregulation of cell surface CD14.
机译：尽管组织在感染过程中同时暴露于外源性和内源性细胞激活介质，但是几乎没有意识到使细胞经受多种介质的作用。我们检查了以下假设：在存在内源性介质肿瘤坏死因子α（TNF）的情况下，中性粒细胞对细菌脂多糖（LPS）的反应发生了显着变化。数据显示，用TNF预处理10至30分钟的人中性粒细胞，对LPS（来自大肠杆菌 K-235或大肠杆菌 0127：B8），以光泽精依赖性化学发光（CL）进行衡量，被视为初始峰值速率的增加以及整个孵育期间累积的总CL的增加。 TNF在1/10 U的TNF / 10 6 中性粒细胞中放大了对LPS的反应，并能够增强对各种浓度LPS（0.01至1,000 ng / ml）的反应。 TNF诱导的LPS反应增加与LPS与嗜中性粒细胞结合增加有关，而抗CD14单克隆抗体可消除这种结合。结果表明，TNF通过细胞表面CD14的上调显着增加LPS诱导的中性粒细胞中氧自由基的释放。

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