Gender dimorphism in trauma-hemorrhage-induced thymocyte apoptosis.
Gender dimorphism in trauma-hemorrhage-induced thymocyte apoptosis.
复制标题
创伤出血诱导的胸腺细胞凋亡中的性别二态性。
DOI：
10.1097/00024382-199910000-00011
复制
发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Chaudry,IH
中科院分区：
文献类型：
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作者：
Angele,MK;Xu,YX;Ayala,A;Schwacha,MG;Catania,RK;Cioffi,WG;Bland,KI;Chaudry,IH
Studies indicate that immune responses after trauma-hemorrhage are significantly depressed in males compared with enhanced immune responses in females under such conditions. Although androgen depletion in male mice by castration before soft tissue trauma and hemorrhagic shock prevents the depression of cell-mediated immunity, the underlying mechanism responsible for this remains unclear. Because the thymus is the primary location of T-cell lymphopoiesis and thymocytes express a large number of androgen receptors, we investigated whether differences in thymic apoptosis might contribute to the divergent immune response in males versus females after trauma-hemorrhage. To study this, male and female C3H/HeN mice were subjected to sham operation or soft tissue trauma (laparotomy) and hemorrhagic shock followed by fluid resuscitation. Animals were killed 72 h thereafter and thymocytes were isolated. Thymocyte interleukin 3 (IL-3) release was significantly suppressed in males, but not females, after trauma-hemorrhage. A parallel increase in thymic apoptosis that was primarily in the CD8+ thymocyte subset was observed in the males. Furthermore, In vitro treatment of thymocytes with 5 [alpha]-dihydrotestosterone (DHT) increased the rate of apoptosis and decreased IL-3 release in a dose-dependent manner. Thus, the gender-dependent dimorphic immune response after trauma-hemorrhage may be in part due to an androgen-induced increase in thymic apoptosis in males under such conditions.
