Endogenous glucocorticoids promote the expansion of myeloid-derived suppressor cells in a murine model of trauma

被引:31
作者
Zhang, Kun [1 ]
Bai, Xiangjun [1 ]
Li, Renjie [1 ]
Xiao, Zhengzheng [2 ]
Chen, Jiajun [1 ]
Yang, Fan [1 ]
Li, Zhanfei [1 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Trauma Surg, Wuhan 430030, Peoples R China
[2] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Neurosurg, Wuhan 430074, Peoples R China
基金
中国国家自然科学基金;
关键词
glucocorticoid; myeloid derived suppressor cells; trauma; ADRENAL INSUFFICIENCY; HYDROCORTISONE; DIFFERENTIATION; ACCUMULATION; INFLAMMATION; STIMULATION; INFECTION; INDUCE;
D O I
10.3892/ijmm.2012.1014
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Stress-dose of glucocorticoid has been demonstrated to be beneficial for trauma patients in clinical studies. Recently, a heterogeneous population of myeloid cells with immunosuppressive activity named myeloid-derived suppressor cells (MDSCs) has been found to accumulate in the trauma host and can be induced by glucocorticoids in vitro. In order to explore the effect of endogenous glucocorticoids on MDSCs under trauma conditions, we blocked the glucocorticoid signal in a murine trauma model using the antagonist of the glucocorticoid receptor RU486 (mifepristone). We found for the first time that RU486 not only blunted MDSC expansion induced by trauma in the spleen, peripheral blood and bone marrow especially at 6 h after traumatic stress but also decreased the survival rate from 100 to 20% in traumatic mice within 7 days. Moreover, neither MDSCs producing arginase-1 nor the morphological characterization of trauma-induced MDSCs was affected by the blockage of the glucocorticoid receptor. Our results suggest that endogenous glucocorticoids may promote MDSCs expansion in a murine trauma model and MDSCs may be beneficial for the trauma host.
引用
收藏
页码:277 / 282
页数:6
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