首页> 外文期刊>Infection and immunity >Leukotriene B4 generation and DNA fragmentation induced by leukocidin from Staphylococcus aureus: protective role of granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF for human neutrophils.
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Leukotriene B4 generation and DNA fragmentation induced by leukocidin from Staphylococcus aureus: protective role of granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF for human neutrophils.

机译:金黄色葡萄球菌中白三烯生成的白三烯B4生成和DNA片段化:粒细胞巨噬细胞集落刺激因子(GM-CSF)和G-CSF对人中性粒细胞的保护作用。

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We studied the effect of leukocidin from Staphylococcus aureus V8 strains (Luk-PV) on the generation of Leukotriene B4 (LTB4) and its metabolites from human polymorphonuclear neutrophils (PMNs). Significant amounts of LTB4 were generated by PMNs after leukocidin exposure in a time- and dose-dependent manner, as shown by reversed-phase high-performance liquid chromatography analysis. In this regard, the S and F components of leukocidin acted synergistically. The calcium ionophore A23187 induced LTB4 generation, and the metabolism of exogenously added LTB4 into biologically less active omega-oxidated compounds was significantly decreased after leukocidin exposure. Priming of PMNs with granulocyte-macrophage colony-stimulating factor (GM-CSF) or G-CSF prior to leukocidin exposure substantially increased toxin- and calcium ionophore A23187-induced LTB4 formation. The inhibitory effects of leukocidin on mediator release were accompanied by membrane damage and DNA fragmentation, which were both restored after pretreatment with GM-CSF. The data suggest that the presence of costimulatory priming factors such as GM-CSF or G-CSF in the microenvironment of an inflammatory focus determines the pathophysiological effects induced by S. aureus leukocidin.
机译:我们研究了金黄色葡萄球菌V8株(Luk-PV)中白细胞介素对白三烯B4(LTB4)及其人类多形核中性粒细胞(PMNs)代谢产物的影响。如反相高效液相色谱分析所示,白细胞介素暴露后,PMN会以时间和剂量依赖性方式产生大量LTB4。在这方面,白血球菌素的S和F成分具有协同作用。钙离子载体A23187诱导了LTB4的生成,并且在暴露白介素后,外源添加的LTB4进入生物活性较低的ω-氧化化合物的代谢显着降低。在暴露白细胞抑制素之前,用粒细胞巨噬细胞集落刺激因子(GM-CSF)或G-CSF引发PMN会大大增加毒素和钙离子载体A23187诱导的LTB4的形成。白细胞抑制素对介质释放的抑制作用伴随着膜损伤和DNA断裂,在用GM-CSF预处理后均得以恢复。数据表明在炎症病灶的微环境中共刺激性启动因子如GM-CSF或G-CSF的存在决定了金黄色葡萄球菌白介素诱导的病理生理作用。

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