BACKGROUND:Activated platelets tether and activate myeloid leukocytes. To investigate the potential relevance of this mechanism in acute myocardial infarction (AMI), we examined cytokine induction by leukocyte-platelet adhesion and the occurrence of leukocyte-platelet conjugates in patients with AMI.

METHODS AND RESULTS:We obtained peripheral venous blood samples in 20 patients with AMI before and daily for 5 days after direct percutaneous transluminal coronary angioplasty (PTCA) and in 20 patients undergoing elective PTCA. Throughout the study period, CD41 immunofluorescence of leukocytes (flow cytometry) revealed increased leukocyte-platelet adhesion in patients with AMI compared with control patients (mean +/- SE of fluorescence [channels] before PTCA: 77 +/- 16 versus 35 +/- 9; P = .003). In vitro, thrombin-stimulated fixed platelets bound to neutrophils and monocytes. Within 2 hours, this resulted in increased mRNA for interleukin (IL),1 beta, IL-8, and monocyte chemoattractant protein (MCP)-1 in unfractionated leukocytes. After 4 hours, IL-1 beta and IL-8 concentration of the cell-free supernatant had increased by 268 +/- 36% and 210 +/- 7%, respectively, and cellular MCP-1 content had increased by 170 +/- 8%. Addition of activated platelets to adherent monocytes had a similar effect and was associated with nuclear factor-kappa B activation. Inhibition of binding by anti-P selectin antibodies reduced the effect of activated platelets on cytokine production.

CONCLUSIONS:In patients with AMI, leukocyte-platelet adhesion is increased. Binding of activated platelets induces IL-1 beta, IL-8, and MCP-1 in leukocytes. Our findings suggest that leukocyte-platelet adhesion contributes to the regulation of inflammatory responses in AMI.

译文

背景:激活血小板束缚并激活髓样白细胞。为了研究该机制在急性心肌梗塞(AMI)中的潜在相关性,我们研究了白细胞-血小板粘附引起的细胞因子诱导以及AMI患者中白细胞-血小板结合物的发生。

方法和结果:我们在20例AMI患者中,分别在直接经皮腔内冠状动脉成形术(PTCA)之前和之后5天以及每天20例接受择期PTCA的患者中获取了外周静脉血。在整个研究过程中,与对照组相比,AMI患者的白细胞CD41免疫荧光(流式细胞仪)显示白细胞-血小板粘附增加(PTCA之前的平均[/ SE]荧光[通道]:77 /-16对35 /-9; P = 0.003)。在体外,凝血酶刺激的固定血小板与嗜中性粒细胞和单核细胞结合。在2小时内,这导致未分离的白细胞中白介素(IL),1β,IL-8和单核细胞趋化蛋白(MCP)-1的mRNA增加。 4小时后,无细胞上清液的IL-1 beta和IL-8浓度分别增加268 /-36%和210 /-7%,细胞MCP-1含量增加170 /-8% 。将活化的血小板添加至粘附的单核细胞具有相似的作用,并且与核因子-κB活化有关。抗P选择素抗体抑制结合可降低活化血小板对细胞因子产生的影响。

结论:在AMI患者中,白细胞-血小板粘附增加。活化血小板的结合在白细胞中诱导IL-1β,IL-8和MCP-1。我们的发现表明,白细胞-血小板粘附有助于调节AMI中的炎症反应。

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