Adherence of neutrophils to cultured human microvascular endothelial cells. Stimulation by chemotactic peptides and lipid mediators and dependence upon the Mac-1, LFA-1, p150,95 glycoprotein family.
Adherence of neutrophils to cultured human microvascular endothelial cells. Stimulation by chemotactic peptides and lipid mediators and dependence upon the Mac-1, LFA-1, p150,95 glycoprotein family.
复制标题
DOI：
10.1172/jci113928
复制
发表时间：
1989-02
期刊：
影响因子：
--
通讯作者：
G. Tonnesen;Donald C. Anderson;T. A. Springer;A. Knedler;N. Avdi;Peter M. Henson
中科院分区：
文献类型：
--
作者：
G. Tonnesen;Donald C. Anderson;T. A. Springer;A. Knedler;N. Avdi;Peter M. Henson
中性粒细胞粘附到微血管内皮并通过微血管内皮迁移的过程是诱导急性炎症反应的早期事件，归因于血管外趋化剂的产生。尽管趋化肽和脂质介质都能在体外和体内增强中性粒细胞的粘附，但循环中性粒细胞和微血管内皮细胞之间相互作用的机制仍不完全清楚。在微量滴定孔粘附测定中，趋化肽 FMLP 和 C5a 以及脂质介质白三烯 B4 (LTB4) 和血小板活化因子 (PAF) 能够以剂量依赖性方式快速增强人中性粒细胞对培养的人微血管内皮细胞以及人脐静脉内皮细胞的粘附。这种刺激的中性粒细胞和培养的人内皮细胞之间的粘附相互作用取决于中性粒细胞表面上Mac-1、LFA-1、p150,95糖蛋白家族的表达，因为与正常对照中性粒细胞相比，白细胞粘附缺陷患者的中性粒细胞缺乏粘附糖蛋白的表面表达，在响应趋化因子刺激时表现出与人内皮细胞的粘附显着减弱。使用针对糖蛋白常见 β 亚基的单克隆抗体 (TS1/18) 通过流式细胞荧光测定法测定，所有四种介质均增强了正常中性粒细胞表面上糖蛋白家族的表达。此外，TS1/18 最多可 100% 抑制正常中性粒细胞与最大浓度 FMLP、C5a、LTB4 或 PAF 刺激的内皮细胞的粘附。此外，HL-60细胞（人早幼粒细胞白血病细胞）既不增加糖蛋白表面表达，也不响应刺激而粘附。因此，急性炎症反应的肽和脂质介质似乎通过依赖于中性粒细胞表面上Mac-1、LFA-1、p150,95糖蛋白家族表达的机制来增强循环中性粒细胞对微血管内皮的粘附。
The process of neutrophil adhesion to and migration through the microvascular endothelium, an early event in the induction of the acute inflammatory response, has been attributed to the generation of extravascular chemoattractants. Although both chemotactic peptides and lipid mediators enhance neutrophil adherence in vitro and in vivo, the mechanism(s) involved in the interaction between circulating neutrophils and microvascular endothelial cells is still not completely understood. In a microtiter well adherence assay, the chemotactic peptides, FMLP and C5a, and the lipid mediators, leukotriene B4 (LTB4) and platelet activating factor (PAF), enhanced human neutrophil adherence to cultured human microvascular endothelial cells as well as to human umbilical vein endothelial cells in a dose-dependent manner with a rapid time course. This stimulated adhesive interaction between neutrophils and cultured human endothelial cells was dependent on the expression of the Mac-1, LFA-1, p150,95 glycoprotein family on the neutrophil surface since neutrophils from patients with leukocyte adhesion deficiency, lacking surface expression of the adhesive glycoproteins, exhibited markedly diminished adherence to human endothelial cells in response to stimulation with chemotactic factors compared to normal control neutrophils. All four mediators enhanced expression of the glycoprotein family on the surface of normal neutrophils as determined by flow cytofluorimetry using a monoclonal antibody (TS1/18) to the glycoprotein common beta subunit. In addition, TS1/18 inhibited up to 100% the adherence of normal neutrophils to endothelial cells stimulated by maximal concentrations of FMLP, C5a, LTB4, or PAF. Moreover, HL-60 cells, human promyelocytic leukemia cells, neither increased glycoprotein surface expression nor adherence in response to stimulation. Thus, peptide and lipid mediators of the acute inflammatory response appear to enhance adherence of circulating neutrophils to the microvascular endothelium by a mechanism dependent on expression of the Mac-1, LFA-1, p150,95 glycoprotein family on the neutrophil surface.