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College of Veterinary Medicine and State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing, China
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-
in the blood of stressed mice were dramatically reduced post Escherichia coli infection or LPS 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.
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1 This work was supported by National Basic Research Program (Project 973) of China Grant 2006CB504303 (to S.J.Z.) and National Natural Science Foundation of China Grants 30725026 and 30671568 (to S.J.Z.).
2 Address correspondence and reprint requests to Dr. Shijun J. Zheng or Dr. Hanchun Yang, College of Veterinary Medicine and State Key Laboratory of Agrobiotechnology, China Agricultural University, 2 Yuanmingyuan West Road, Beijing 100193, China. E-mail addresses: sjzheng{at}cau.edu.cn and yanghanchun1{at}cau.edu.cn
3 Abbreviations used in this paper: G–, Gram negative; DEX, dexamethasone; EIA, enzyme immunoassay; G+, Gram positive; GILZ, glucocorticoid-induced leucine zipper.
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