RAPID INDUCTION OF NEUTROPHIL ENDOTHELIAL ADHESION BY ENDOTHELIAL COMPLEMENT-FIXATION
RAPID INDUCTION OF NEUTROPHIL ENDOTHELIAL ADHESION BY ENDOTHELIAL COMPLEMENT-FIXATION
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DOI：
10.1038/339314a0
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发表时间：
1989-05-25
期刊：
影响因子：
64.8
通讯作者：
WARD, PA
中科院分区：
文献类型：
--
作者：
MARKS, RM;TODD, RF;WARD, PA
中性粒细胞与血管内皮的粘附是其进入急性炎症病变的早期事件1。在评价急性炎症中潜在的嗜酸性粒细胞-内皮粘附机制时，重要的考虑因素是损伤后体内粘附可能发生得非常快2 - 4，并且反应的特异性在于改变的内皮5。也就是说，嗜中性粒细胞仅粘附于邻近炎症病灶的改变的内皮，而不是随机粘附，如如果嗜中性粒细胞的活化是粘附的起始物所预期的那样。我们已经探索了一种可能的桥梁作用，补体引起早期嗜中性粒细胞-内皮细胞粘附。补体系统参与炎症过程，能够快速扩增，并且炎症部位的内皮补体固定可产生中性粒细胞粘附的内皮限制性信号。我们现在已经开发了一种模型，在该模型中，通过构建一种新的分子，内皮结合凝集素Ulex europaeus I（参考文献6）和补体激活剂眼镜蛇毒因子7，8的杂交体，可以在没有复杂因素（如免疫球蛋白沉积）的情况下进行研究。该分子具有使补体固定在人脐静脉内皮细胞上的能力。我们发现，补体结合是一个强大的和快速的刺激中性粒细胞粘附。神经元粘附仅需要C3的内皮沉积，并且通过3型补体受体介导。
THE adhesion of neutrophils to vascular endothelium is an early event in their recruitment into acute inflammatory lesions1. In evaluating potential neutrophil–endothelial adhesive mechanisms in acute inflammation, important considerations are that adhesionin vivomay occur very rapidly following injury2–4and that the specificity of the reaction resides in altered endothelium5. That is, neutrophils adhere only to altered endothelium adjacent to an inflammatory focus, rather than at random as would be expected if activation of neutrophils were the initiator of adhesion. We have explored a possible bridging role for complement in causing early neutrophil–endothelial cell adhesion. The complement system is involved in inflammatory processes, is capable of rapid amplification, and endothelial complement fixation at sites of inflammation could generate an endothelium-restricted signal for neutrophil adhesion. We have now developed a model in which this can be investigated without complicating factors such as immunoglobulin deposition, by constructing a novel molecule, a hybrid of the endothelial binding lectinUlex europaeusI (ref. 6) and of the complement activator cobra venom factor7,8. This molecule has the capacity to cause fixation of complement on human unbilical vein endothelial cells. We show that complement fixation is a potent and rapid stimulus for neutrophil adhesion. Neutrophil adhesion requires only endothelial deposition of C3, and is mediated through the type 3 complement receptor.