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首页> 外文期刊>Journal of Cellular Physiology >α Mβ 2-integrin-intercellular adhesion molecule-1 interactions drive the flow-dependent trafficking of Guillain-Barré syndrome patient derived mononuclear leukocytes at the blood-nerve barrier in vitro
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α Mβ 2-integrin-intercellular adhesion molecule-1 interactions drive the flow-dependent trafficking of Guillain-Barré syndrome patient derived mononuclear leukocytes at the blood-nerve barrier in vitro

机译：Mαβ2-integrin-intercellular粘附molecule-1交互驱动flow-dependent贩卖格林-巴利综合征的病人单核白细胞2屏障在体外

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The mechanisms of hematogenous leukocyte trafficking at the human blood-nerve barrier (BNB) are largely unknown. Intercellular adhesion molecule-1 (ICAM-1) has been implicated in the pathogenesis of Guillain-Barré syndrome (GBS). We developed a cytokine-activated human in vitro BNB model using primary endoneurial endothelial cells. Endothelial treatment with 10U/ml tissue necrosis factor-α and 20U/ml interferon-γ resulted in de novo expression of pro-inflammatory chemokines CCL2, CXCL9, CXCL11, and CCL20, with increased expression of CXCL2-3, CXCL8, and CXCL10 relative to basal levels. Cytokine treatment induced/enhanced ICAM-1, E- and P-selectin, vascular cell adhesion molecule-1 and the alternatively spliced pro-adhesive fibronectin variant, fibronectin connecting segment-1 expression in a time-dependent manner, without alterations in junctional adhesion molecule-A expression. Lymphocytes and monocytes from untreated GBS patients express ICAM-1 counterligands, α M- and α L-integrin, with differential regulation of α M-integrin expression compared to healthy controls. Under flow conditions that mimic capillary hemodynamics in vivo, there was a 3-fold increase in total GBS patient and healthy control mononuclear leukocyte adhesion/migration at the BNB following cytokine treatment relative to the untreated state. Function neutralizing monoclonal antibodies against human α M-integrin (CD11b) and ICAM-1 reduced untreated GBS patient mononuclear leukocyte trafficking at the BNB by 59% and 64.2%, respectively. Monoclonal antibodies against α L-integrin (CD11a) and human intravenous immunoglobulin reduced total leukocyte adhesion/migration by 22.8% and 17.6%, respectively. This study demonstrates differential regulation of α M-integrin on circulating mononuclear cells in GBS, as well as an important role for α M-integrin-ICAM-1 interactions in pathogenic GBS patient leukocyte trafficking at the human BNB in vitro.
机译：血性的白细胞的机制贩卖人口的2障碍(BNB)在很大程度上是未知的。molecule-1 (ICAM-1)被卷入格林-巴利综合征(GBS)的发病机理。开发了一种人类体外BNB cytokine-activated模型使用主endoneurial内皮细胞。坏死因子-α和20 u /毫升干扰素-γ导致新创的表达促炎症趋化因子CCL2, CXCL9 CXCL11,和CCL20 CXCL2-3的表达增加,CXCL8, CXCL10相对于基底的水平。细胞因子治疗诱导/增强ICAM-1, E -和血管细胞粘附molecule-1 P-selectin或者拼接pro-adhesive纤连蛋白变体,纤连蛋白连接段1表达时间的方式,在不改变交叉的附着力分子—表达式。未经处理的GBS患者表达ICAM-1counterligands、α-和αL-integrin,微分调节αM-integrin表达与健康对照组相比。流条件,模拟毛细血管血液动力学体内,在三倍增加GBS患者和健康控制单核在BNB后白细胞粘附和迁移细胞因子治疗相对于未经处理的状态。人类α抗体M-integrin (CD11b)和ICAM-1减少未经处理的GBS患者单核细胞在BNB 59%和白细胞贩卖64.2%,分别。对αL-integrin (CD11a)和人类静脉注射免疫球蛋白减少总白细胞粘附/迁移了22.8%和17.6%,分别。微分调节αM-integrin在GBS循环单核细胞,以及一个重要的角色为αM-integrin-ICAM-1交互在致病性GBS患者白细胞在人类BNB体外贩卖。

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