Enhanced resistance of restraint-stressed mice to sepsis
Enhanced resistance of restraint-stressed mice to sepsis
复制标题
束缚应激小鼠对败血症的抵抗力增强
DOI：
10.4049/jimmunol.181.5.3441
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发表时间：
2008-09-01
影响因子：
4.4
通讯作者：
Zheng, Shijun J.
中科院分区：
文献类型：
--
作者：
Wang, Yu;Lu, Ying;Zheng, Shijun J.
脓毒症仍然是世界各地的主要健康问题。应激对宿主抵抗脓毒症的影响尚不十分清楚。为了探讨慢性应激对脓毒症的影响，我们研究了束缚应激对小鼠抵抗脓毒症的影响。有趣的是，发现束缚应激增强了小鼠的抗菌抗性，并且与对照组相比，大肠杆菌感染或LIPS处理后应激小鼠血液中促炎细胞因子IL-1、IL-6、IL-12和TNF-α的浓度显著降低（p < 0.05）。此外，糖皮质激素诱导的亮氨酸拉链（GILZ）的mRNA表达上调的小鼠脾脏和腹腔巨噬细胞受到束缚应激或地塞米松治疗。这些结果表明，束缚应激增强了小鼠对脓毒症的抵抗力，支持脓毒症的皮质疗法，并提出束缚应激小鼠作为动物模型来阐明应激相关的抗菌药物抵抗的机制。
Sepsis remains a major health concern across the world. The effects of stress on host resistance to sepsis are still not very clear. To explore the effects of chronic stress on sepsis, we examined the impact of restraint stress on the resistance of mice to sepsis. Interestingly, it was found that restraint stress enhanced the antisepsis resistance of mice and the concentrations of the proinflammatory cytokines IL-1, IL-6, IL-12, and TNF-alpha in the blood of stressed mice were dramatically reduced post Escherichia coli infection or LIPS treatment as compared with that of controls (p < 0.05). In addition, the mRNA expressions of glucocorticoid-induced leucine zipper (GILZ) were up-regulated in the spleen and peritoneal macrophages of mice receiving restraint stress or dexamethasone treatment. These results demonstrate that restraint stress enhances the resistance of mice to sepsis, supporting corticotherapy for sepsis and proposing restraint-stressed mouse as an animal model to elucidate mechanisms of stress-associated, antisepsis resistance.