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首页> 外文期刊>Infection and immunity >Selective killing of human monocytes and cytokine release provoked by sphingomyelinase (beta-toxin) of Staphylococcus aureus.
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Selective killing of human monocytes and cytokine release provoked by sphingomyelinase (beta-toxin) of Staphylococcus aureus.

机译：用金黄色葡萄球菌的鞘氨酰胺酶（β-毒素）引发的人单核细胞和细胞因子的选择性杀害。

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The best-known activity of Staphylococcus aureus sphingomyelinase C, alias beta-toxin, is as a hemolysin that provokes hot-cold lysis of erythrocytes which contain substantial amounts of sphingomyelin in the plasma membrane. Sheep erythrocytes are most susceptible, and we found that one hemolytic unit, representing the toxin concentration that elicits 50% hemolysis of 2.5 X 10(8) erythrocytes per ml, corresponds to 0.05 enzyme units or to approximately 0.25 microg of sphingomyelinase per ml. The cytotoxic action of beta-toxin on nucleated cells has not been described in any detail before, and the present investigation was undertaken to fill this information gap. We now identify beta-toxin as a remarkably potent monocytocidal agent. At a concentration of 0.001 U/ml, corresponding to approximately 5 ng/ml, beta-toxin killed over 50% of human monocytes (10(6) cells per ml) within 60 min. By contrast, 1 to 5 microg of beta-toxin per ml had no cytocidal effects on human granulocytes, fibroblasts, lymphocytes, or erythrocytes. A selective monocytocidal action was also observed with sphingomyelinase C from Bacillus cereus and a Streptomyces sp., whereas phospholipase A2 and phospholipase D at 100 U/ml were without effect. Monocytes succumbing to the action of beta-toxin processed and released interleukin-1beta, soluble interleukin-6 receptor, and soluble CD14 into the supernatant. Thus, monocyte killing by beta-toxin is associated with cytokine-related events that are important for the initiation and progression of infectious disease. These findings uncover a potentially important role for sphingomyelinase as a determinant of microbial pathogenicity.
机译：金黄色葡萄球菌鞘磷脂酶C，别名β-毒素的最着名的活性作为溶血素，其引起红细胞的热冷裂解，其在血浆膜中含有大量的鞘氨酰胺。绵羊红细胞最容易受到影响，我们发现一种溶血单元，代表毒素浓度，其溶血浓度为每mL的2.5×10（8）个红细胞的50％溶血，对应于0.05个酶单位或每mL约0.25微米的鞘氨基氨基酶。之前没有详细描述β-毒素对核细胞的细胞毒性作用，并进行了本调查以填补这一信息差距。我们现在将β-毒素鉴定为一个非常有效的单核特子剂。以0.001u / ml的浓度，对应于约5ng / ml，β-毒素在60分钟内造成超过50％的人单核细胞（每mL 10（6）个细胞）。相比之下，每mL的1至5微米的β-毒素对人粒细胞，成纤维细胞，淋巴细胞或红细胞没有细胞癌。还通过来自芽孢杆菌和链霉菌Sp的鞘氨基氨基酶C观察到选择性单核特异性作用。，磷脂酶A2和100u / ml的磷脂酶D没有效果。单核细胞屈服于β-毒素加工和释放的白细胞介素-1β，可溶性白细胞介素-6受体和可溶性CD14进入上清液中的作用。因此，通过β-毒素的单核细胞杀死与细胞因子相关的事件有关，这对传染病的起始和进展很重要。这些发现发现鞘氨基酶酶作为微生物致病性的决定性的潜在重要作用。

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