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首页> 外文期刊>Infection and immunity >Interleukins 6 and 11 protect mice from mortality in a staphylococcal enterotoxin-induced toxic shock model.
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Interleukins 6 and 11 protect mice from mortality in a staphylococcal enterotoxin-induced toxic shock model.

机译：在葡萄球菌肠毒素诱导的毒性休克模型中，白介素6和11保护小鼠免于死亡。

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BALB/By mice given doses of D-galactosamine plus Staphylococcus aureus enterotoxin B die within 48 h of administration. The cause of death is a syndrome much like toxic shock syndrome in humans. We used this model to investigate the role of two cytokines, interleukin 6 and interleukin 11, which share the signal transducing subunit, gp130, of their respective receptors. We observed that pretreatment of mice with antibody to interleukin 6 increased mortality from 55% to nearly 90% (P < 0.001), while pretreatment with either cytokine reduced death. The protection was dose dependent; however, interleukin 6 was about 10-fold more potent that interleukin 11. These data indicate that endogenous interleukin 6 plays a protective role in attenuating acute inflammatory responses; furthermore, interleukin 6 and interleukin 11 can abrogate T-cell activation due to triggering by superantigen. A possible clinical role for these cytokines in the treatment of toxic shock merits further investigation.
机译：给予D-半乳糖胺加金黄色葡萄球菌肠毒素B剂量的BALB / By小鼠在给药后48小时内死亡。死亡原因是一种类似于人类中毒性休克综合症的综合症。我们使用该模型研究了两种细胞因子，白细胞介素6和白细胞介素11的作用，它们共享各自受体的信号转导亚基gp130。我们观察到，用白介素6抗体对小鼠进行预处理可使死亡率从55％增至近90％（P <0.001），而用任一种细胞因子进行预处理均可降低死亡率。保护是剂量依赖性的;然而，白介素6的效力比白介素11高约10倍。这些数据表明，内源性白介素6在减轻急性炎症反应中起保护作用。此外，由于超抗原的触发，白介素6和白介素11可以消除T细胞活化。这些细胞因子在中毒性休克治疗中可能的临床作用值得进一步研究。

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