Grau A J, Reis A, Buggle F, Al-Khalaf A, Werle E, Valois N, Bertram M, Becher H, Grond-Ginsbach C
Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, 69120 Heidelberg, Germany.
J Neurol Sci. 2001 Nov 15;192(1-2):41-7. doi: 10.1016/s0022-510x(01)00590-1.
Activated monocytes may contribute to the pathogenesis of ischemic stroke. We tested the hypothesis that release products and procoagulant activity of monocytes are increased in acute ischemic stroke. In patients on days 1, 3 and 7 after ischemic stroke and in age- and sex-matched healthy control subjects, we assessed plasma levels of interleukin 8 (IL-8) and neopterin (enzyme linked immunosorbent assay, ELISA) and investigated superoxidanion release (ferricytochrome C reduction), procoagulant activity (one-stage clotting assay) and tissue factor (TF) gene transcription (reverse transcriptase polymerase chain reaction) by monocytes. As compared to control subjects (n=23), IL-8 levels were increased on day 1 after stroke (n=22; p=0.005) and remained elevated on days 3 and 7. Neopterin levels were elevated on days 3 and 7 (p<0.05, respectively) but not on day 1. Neopterin and IL-8 were not correlated with monocyte counts. Superoxid anion production by stimulated and unstimulated monocytes was not different between groups. TF mRNA could neither be detected in monocytes from patients investigated within 12 h after ischemia (n=12) nor in control subjects (n=10) and procoagulant activity of cells was similar in both groups. Our results indicate increased monocyte activation after ischemic stroke although not all activation parameters were elevated. We found no support for the hypothesis that circulating monocytes express TF and possess increased procoagulant activity. Elevated IL-8 may contribute to stroke pathophysiology by activating polymorphonuclear leukocyte (PMNL) activation early after ischemia.
活化的单核细胞可能参与缺血性脑卒中的发病机制。我们验证了急性缺血性脑卒中时单核细胞释放产物及促凝活性增加这一假说。在缺血性脑卒中后第1天、第3天和第7天的患者以及年龄和性别匹配的健康对照者中，我们评估了血浆白细胞介素8（IL-8）和新蝶呤水平（酶联免疫吸附测定，ELISA），并研究了单核细胞的超氧阴离子释放（高铁细胞色素C还原法）、促凝活性（一步凝血测定法）及组织因子（TF）基因转录（逆转录聚合酶链反应）。与对照者（n = 23）相比，脑卒中后第1天患者（n = 22；p = 0.005）的IL-8水平升高，且在第3天和第7天仍维持在较高水平。新蝶呤水平在第3天和第7天升高（p分别<0.05），但在第1天未升高。新蝶呤和IL-8与单核细胞计数无关。刺激组和未刺激组单核细胞产生的超氧阴离子在两组间无差异。在缺血后12小时内研究的患者（n = 12）及对照者（n = 10）的单核细胞中均未检测到TF mRNA，两组细胞的促凝活性相似。我们的结果表明，缺血性脑卒中后单核细胞活化增加，尽管并非所有活化参数均升高。我们没有找到支持循环单核细胞表达TF并具有增强促凝活性这一假说的证据。缺血后早期，升高的IL-8可能通过激活多形核白细胞（PMNL）活化而参与脑卒中的病理生理过程。
