首页> 外文会议>7th China-Japan International Congress of Microbiology Shanghai Symposium-2000 4-6 August 2000 Shanghai >Effect of CV6209, A platelet-activating factor antagonist, on shiga toxin-induced tumor necrosis factor-alpha expression in human monocytic cells
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Effect of CV6209, A platelet-activating factor antagonist, on shiga toxin-induced tumor necrosis factor-alpha expression in human monocytic cells

机译:血小板活化因子拮抗剂CV6209对芝加毒素诱导的人单核细胞中肿瘤坏死因子-α表达的影响

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摘要

The haemolytic ueaemic syndrome (HUS) is often associated with infection by enterhemorrhagic Escherichia coli (EHEC) that produce Shiga toxin (Stx). Stx is thought to damage human endothelial cells and lead to HUS. A number of observations indicate that cytokines, in particular tumor necrosis factor (TNF)-alpha, contribute to this pathologic process in HUS, since it regulates endothelial cell membrane expression of a glycolipid globotriaosylceramide (Gb3), which serves as the Stx receptor. The degree of HuS is closely related to levels of TNF-alpha. In this study, we investigated whether CV6209, a platelet-activating factor (PAF) antagonist, could modulate Stx-induced TNF-alpha production in human monocytic cells.
机译:溶血性尿毒症综合征(HUS)通常与产生志贺毒素(Stx)的肠出血性大肠杆菌(EHEC)感染有关。人们认为Stx会损害人类内皮细胞并导致HUS。许多观察结果表明,细胞因子,特别是肿瘤坏死因子(TNF)-α参与了HUS的这种病理过程,因为它调节了糖脂球果糖神经酰胺(Gb3)的内皮细胞膜表达,而糖脂球蛋白是神经酰胺,它是Stx受体。 HuS的程度与TNF-α的水平密切相关。在这项研究中,我们调查了血小板活化因子(PAF)拮抗剂CV6209是否可以调节人单核细胞中Stx诱导的TNF-α产生。

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