首页> 美国卫生研究院文献>Infection and Immunity >Phospholipid metabolism induced by Clostridium perfringens alpha-toxin elicits a hot-cold type of hemolysis in rabbit erythrocytes.
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Phospholipid metabolism induced by Clostridium perfringens alpha-toxin elicits a hot-cold type of hemolysis in rabbit erythrocytes.

机译:产气荚膜梭菌α-毒素诱导的磷脂代谢在兔红细胞中引起了一种热-冷型溶血。

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摘要

GTP and AIF4- significantly stimulated the late phosphatidic acid (PA) formation induced by Clostridium perfringens alpha-toxin in rabbit erythrocyte lysates. Pertussis toxin blocked the PA production. AIF4- markedly enhanced phosphatidylethanol production induced by alpha-toxin in the presence of ethanol. GTP[gamma S] stimulated the PA formation and hemolysis induced by alpha-toxin, and GDP[beta S] inhibited them. An H-to-G mutation at position 126 (H126G) induced the PA formation and hemolysis in a Co2+ concentration-dependent manner. H148G induced neither the PA formation nor hemolysis. These results suggest that the toxin-induced hemolysis is due to activation of phospholipid metabolism systems through GTP-binding protein.
机译:GTP和AIF4-显着刺激了产气荚膜梭菌α-毒素在兔红细胞裂解液中诱导的晚期磷脂酸(PA)的形成。百日咳毒素阻止了PA的产生。在乙醇存在下,AIF4-明显增强了由α-毒素诱导的磷脂酰乙醇的产生。 GTP [γS]刺激了α毒素诱导的PA形成和溶血,而GDP [βS]则抑制了它们。位置126处的H到G突变(H126G)以Co2 +浓度依赖性方式诱导PA的形成和溶血。 H148G既不诱导PA形成也不引起溶血。这些结果表明,毒素诱导的溶血是由于通过GTP结合蛋白激活的磷脂代谢系统。

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