Sulfatide Attenuates Experimental Staphylococcus aureus Sepsis through a CD1d-Dependent Pathway
Sulfatide Attenuates Experimental Staphylococcus aureus Sepsis through a CD1d-Dependent Pathway
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DOI：
10.1128/iai.01334-12
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发表时间：
2013-04-01
影响因子：
3.1
通讯作者：
Jin, Tao
中科院分区：
文献类型：
--
作者：
Kwiecinski, Jakub;Rhost, Sara;Jin, Tao
自然杀伤T（NKT）淋巴细胞参与对微生物感染的早期反应。此外，硫苷脂，髓鞘自身鞘糖脂，激活II型NKT细胞亚群，并可以调节鼠模型中的疾病。我们在金黄色葡萄球菌败血症小鼠模型中研究了NKT细胞的作用和硫苷脂治疗的效果。缺乏CD 1d限制性NKT细胞并没有改变致死接种S.金黄色。相比之下，硫苷脂治疗显著提高了S.金黄色葡萄球菌脓毒症，伴随血液中肿瘤坏死因子α和白细胞介素-6水平降低。硫苷脂治疗的保护作用依赖于CD 1d，而不是I型NKT细胞，这表明硫苷脂激活II型NKT细胞对S.金黄色葡萄球菌脓毒症。
Natural killer T (NKT) lymphocytes are implicated in the early response to microbial infection. Further, sulfatide, a myelin self-glycosphingolipid, activates a type II NKT cell subset and can modulate disease in murine models. We examined the role of NKT cells and the effect of sulfatide treatment in a murine model of Staphylococcus aureus sepsis. The lack of CD1d-restricted NKT cells did not alter survival after a lethal inoculum of S. aureus. In contrast, sulfatide treatment significantly improved the survival rate of mice with S. aureus sepsis, accompanied by decreased levels of tumor necrosis factor alpha and interleukin-6 in the blood. The protective effect of sulfatide treatment depended on CD1d but not on type I NKT cells, suggesting that activation of type II NKT cells by sulfatide has beneficial effects on the outcome of S. aureus sepsis in this model.