Neutrophil adherence to isolated adult cardiac myocytes. Induction by cardiac lymph collected during ischemia and reperfusion.
Neutrophil adherence to isolated adult cardiac myocytes. Induction by cardiac lymph collected during ischemia and reperfusion.
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中性粒细胞粘附于分离的成体心肌细胞。
DOI：
10.1172/jci115626
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Entman,ML
中科院分区：
文献类型：
--
作者：
Youker,K;Smith,CW;Anderson,DC;Miller,D;Michael,LH;Rossen,RD;Entman,ML
犬中性粒细胞可以通过用趋化因子如酵母聚糖激活血清（ZAS）刺激中性粒细胞来诱导体外粘附于分离的成年心肌细胞，前提是心肌细胞先前已暴露于细胞因子如白细胞介素1（IL-1）或肿瘤坏死因子-α。这些细胞因子诱导细胞间粘附分子-1（ICAM-1）在心肌细胞上的合成和表面表达，并且中性粒细胞粘附几乎完全依赖于CD 18和ICAM-1。本研究探讨心脏特异性淋巴液收集清醒的狗在1小时冠状动脉闭塞和3天的再灌注诱导心肌细胞ICAM-1的表达，和嗜中性粒细胞-心肌细胞粘附的能力。再灌注淋巴液诱导ICAM-1在离体心肌细胞中表达，并诱导心肌细胞粘附ZAS刺激的中性粒细胞，抗CD 18和抗ICAM-1单克隆抗体完全抑制。这种活性在再灌注90 min时达到峰值，并持续长达72 h。缺血前淋巴液无刺激性。IL-1似乎不是淋巴中的刺激因子，因为发现淋巴稀释液抑制重组IL-1 β的刺激作用。然而，白细胞介素6（IL-6）的研究表明，重组IL-6刺激心肌细胞对ZAS刺激的中性粒细胞的增殖（ED 50 = 0.002 U/ml）和ICAM-1的表达由分离的心肌细胞。IL-6中和抗体显著降低再灌注淋巴液刺激粘附和ICAM-1表达的能力，估计再灌注淋巴液中IL-6的水平为0.035 ~ 0.14 U/ml。这些结果表明，缺血心肌再灌注期间细胞外液中存在能够促进中性粒细胞与心肌细胞粘附的细胞因子，其中一种细胞因子是IL-6。中性粒细胞-肌细胞粘附可能具有致病意义，因为它可能增强中性粒细胞的细胞毒活性。图片
Canine neutrophils can be induced to adhere in vitro to isolated adult cardiac myocytes by stimulation of the neutrophils with chemotactic factors such as zymosan-activated serum (ZAS) only if the myocytes have been previously exposed to cytokines such as interleukin 1 (IL-1) or tumor necrosis factor-alpha. These cytokines induce synthesis and surface expression of intercellular adhesion molecule-1 (ICAM-1) on the myocyte, and neutrophil adhesion is almost entirely CD18 and ICAM-1 dependent. The present study examines cardiac-specific lymph collected from awake dogs during 1-h coronary occlusion and 3 d of reperfusion for its ability to induce both ICAM-1 expression in cardiac myocytes, and neutrophil-myocyte adherence. Reperfusion lymph induced ICAM-1 expression in isolated myocytes, and myocyte adherence to ZAS-stimulated neutrophils that was completely inhibited by anti-CD18 and anti-ICAM-1 monoclonal antibodies. This activity peaked at 90 min of reperfusion and persisted for up to 72 h. Preischemic lymph was not stimulatory. IL-1 appeared not to be a stimulating factor in lymph in that dilutions of lymph were found to inhibit the stimulatory effects of recombinant IL-1 beta. However, investigation of interleukin 6 (IL-6) revealed that recombinant IL-6 stimulated myocyte adhesiveness for ZAS-stimulated neutrophils (ED50 = 0.002 U/ml) and expression of ICAM-1 by isolated myocytes. IL-6 neutralizing antibody markedly reduced the ability of reperfusion lymph to stimulate adhesion and ICAM-1 expression, and estimates of levels of IL-6 in reperfusion lymph ranged from 0.035 to 0.14 U/ml. These results indicate that cytokines capable of promoting neutrophil-myocyte adhesion occur in extracellular fluid during reperfusion of ischemic myocardium, and that one of these cytokines is IL-6. Neutrophil-myocyte adhesion may be of pathogenic significance because it may enhance the cytotoxic activity of the neutrophil.Images