Monokines mediate decreased hepatic glucocorticoid binding in endotoxemia.
Monokines mediate decreased hepatic glucocorticoid binding in endotoxemia.
复制标题
单核因子介导内毒素血症中肝脏糖皮质激素结合减少。
DOI：
10.1002/jlb.41.3.236
复制
发表时间：
1987
影响因子：
5.5
通讯作者：
McCallum,RE
中科院分区：
文献类型：
--
作者：
Hill,MR;Stith,RD;McCallum,RE
本研究的目的是确定内毒素是否通过介体的作用降低肝糖皮质激素结合。在C3 HeB/FeJ LPS正常反应小鼠和C3 H/HeJ LPS低反应小鼠中测定了肝脏胞液中的类固醇结合、血糖水平和血浆皮质酮水平。在C3 HeB/FeJ小鼠中，内毒素显著降低类固醇结合位点的最大数量（Bmax）至对照的30%。血浆葡萄糖水平降低至对照组的50%，血浆皮质酮水平升高4倍。在给予内毒素的C3 H/HeJ小鼠中未观察到这些参数的变化，但在最高剂量的内毒素下血糖水平降低。在接受C3 HeB/FeJ腹膜渗出液细胞（用硫乙醇酸盐诱导）和内毒素后4-6小时，在C3 H/HeJ小鼠中观察到类固醇结合减少。在接受C3 H/HeJ腹膜渗出液细胞和内毒素的C3 H/HeJ小鼠中未观察到类固醇结合的变化。CF-1小鼠用1 × 107 BCG感染，2周后用内毒素（2 μg）攻击2 h，产生富含介体的血浆。BCG-内毒素血浆转移到C3 H/HeJ小鼠也导致类固醇结合和血糖降低。这些结果表明内毒素休克时糖皮质激素作用的扰动是由内毒素以外的可溶性因子介导的。一种可能的介质来源是单核吞噬细胞。
The purpose of this study was to determine whether endotoxin decreased hepatic glucocorticoid binding by the action of mediator(s). Steroid binding in liver cytosol, plasma glucose levels, and plasma corticosterone levels were assayed in C3HeB/FeJ LPS normoresponsive and C3H/HeJ LPS hyporesponsive mice. In C3HeB/FeJ mice, endotoxin significantly depressed the maximum number of steroid binding sites (Bmax) to 30% of control. Plasma glucose levels were decreased to 50% of control, and plasma corticosterone levels increased 4-fold. No changes in these parameters were seen in C3H/HeJ mice given endotoxin, except for decreased plasma glucose levels at the highest dose of endotoxin. Decreased steroid binding was observed in C3H/HeJ mice 4-6 hours after receiving C3HeB/FeJ peritoneal exudate cells (elicited with thiogiycollate) and endotoxin. No change in steroid binding was observed in C3H/HeJ mice that received C3H/HeJ peritoneal exudate cells and endotoxin. Mediator-rich plasma was produced in CF-1 mice by infecting them with 1 x 107BCG and by challenging them with endotoxin (2 μg) 2 weeks later for 2 h. Transfer of BCG-endotoxin plasma to C3H/HeJ mice also resulted in decreased steroid binding and plasma glucose. These results indicate that perturbation of glucocorticoid action during endotoxin shock is mediated by soluble factor(s) other than endotoxin. A likely source of mediator(s) is the mononuclear phagocyte.