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Direct Activation of Human Endothelial Cells by Plasmodium falciparum-Infected Erythrocytes

机译：恶性疟原虫感染的红细胞直接激活人内皮细胞

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Cytoadherence of Plasmodium falciparum-infected erythrocytes (PRBC) to endothelial cells causes severe clinical disease, presumably as a of result perfusion failure and tissue hypoxia. Cytoadherence to endothelial cells is increased by endothelial cell activation, which is believed to occur in a paracrine fashion by mediators such as tumor necrosis factor alpha (TNF-α) released from macrophages that initially recognize PRBC. Here we provide evidence that PRBC directly stimulate human endothelial cells in the absence of macrophages, leading to increased expression of adhesion-promoting molecules, such as intercellular adhesion molecule 1. Endothelial cell stimulation by PRBC required direct physical contact for a short time (30 to 60 min) and was correlated with parasitemia. Gene expression profiling of endothelial cells stimulated by PRBC revealed increased expression levels of chemokine and adhesion molecule genes. PRBC-stimulated endothelial cells especially showed increased expression of molecules involved in parasite adhesion but failed to express molecules promoting leukocyte adhesion, such as E-selectin and vascular cell adhesion molecule 1, even after challenge with TNF-α. Collectively, our data suggest that stimulation of endothelial cells by PRBC may have two effects: prevention of parasite clearance through increased cytoadherence and attenuation of leukocyte binding to endothelial cells, thereby preventing deleterious immune reactivity.
机译：恶性疟原虫感染的红细胞（PRBC）对内皮细胞的细胞粘附会导致严重的临床疾病，大概是由于灌注失败和组织缺氧所致。内皮细胞活化增强了对内皮细胞的细胞粘附，据信这是通过旁分泌的方式发生的，例如通过从最初识别PRBC的巨噬细胞释放的肿瘤坏死因子α（TNF-α）等介体以旁分泌的方式发生。在这里，我们提供的证据表明PRBC在不存在巨噬细胞的情况下直接刺激人内皮细胞，从而导致粘附促进分子（例如细胞间粘附分子1）的表达增加。PRBC刺激内皮细胞需要短时间直接物理接触（30到30 60分钟），并与寄生虫病相关。 PRBC刺激的内皮细胞的基因表达谱显示趋化因子和粘附分子基因的表达水平增加。 PRBC刺激的内皮细胞尤其显示出参与寄生虫粘附的分子的表达增加，但是即使在受到TNF-α攻击后，也未能表达促进白细胞粘附的分子，例如E-选择素和血管细胞粘附分子1。总体而言，我们的数据表明PRBC刺激内皮细胞可能具有两种作用：通过增加细胞粘附性来防止寄生虫清除以及减弱白细胞与内皮细胞的结合，从而防止有害的免疫反应。

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