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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Inhibition of neutrophil-mediated production of reactive oxygen species (ROS) by endothelial cells is not impaired in anti-neutrophil cytoplasmic autoantibodies (ANCA)-associated vasculitis patients.
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Inhibition of neutrophil-mediated production of reactive oxygen species (ROS) by endothelial cells is not impaired in anti-neutrophil cytoplasmic autoantibodies (ANCA)-associated vasculitis patients.

机译：在抗中性粒细胞胞浆自身抗体（ANCA）相关的血管炎患者中，内皮细胞对中性粒细胞介导的活性氧（ROS）产生的抑制作用不会受到损害。

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Leucocyte transendothelial migration is strictly regulated to prevent undesired inflammation and collateral damage of endothelial cells by activated neutrophils/monocytes. We hypothesized that in anti-neutrophil cytoplasmic autoantibodies (ANCA)-associated vasculitis (AAV) patients' dysregulation of this process might underlie vascular inflammation. Peripheral blood mononuclear cells (PBMC) and neutrophils from AAV patients (n = 12) and healthy controls (HC, n = 12) were isolated. The influence of human umbilical vein endothelial cells (HUVEC) on neutrophil/monocytes function was tested by N-formyl-methionyl-leucyl-phenyl-alanine (fMLP)- and phorbol 12-myristate 13-acetate (PMA)-mediated ROS production, degranulation and interleukin (IL)-8 production. In addition, the ability of lipopolysaccharide (LPS)-stimulated PBMC to produce tumour necrosis factor (TNF)-alpha in the presence or absence of HUVEC was tested. HUVEC inhibited ROS production dose-dependently by fMLP-stimulated neutrophils but did not influence degranulation. No differences between neutrophils from HC and AAV were found. However, in only one active patient was degranulation inhibited significantly by HUVEC only before cyclophosphamide treatment, but not 6 weeks later. Co-cultures of HUVEC with LPS-stimulated neutrophils/monocytes increased IL-8 production while TNF-alpha production was inhibited significantly. There was no apparent difference between AAV patients and HC in this respect. Our findings demonstrate that HUVEC are able to inhibit ROS and modulate cytokine production upon stimulation of neutrophils or monocytes. Our data do not support the hypothesis that endothelial cells inhibit ROS production of neutrophils from AAV patients inadequately. Impaired neutrophil degranulation may exist in active patients, but this finding needs to be confirmed.
机译：严格调节白细胞跨内皮迁移，以防止活化的嗜中性粒细胞/单核细胞对血管内皮细胞产生不希望的炎症和附带损害。我们假设在抗中性粒细胞胞浆自身抗体（ANCA）相关血管炎（AAV）中，患者对该过程的失调可能是血管炎症的基础。分离了AAV患者（n = 12）和健康对照（HC，n = 12）的外周血单个核细胞（PBMC）和中性粒细胞。通过N-甲酰基-甲硫酰基-亮氨酰-苯基丙氨酸（fMLP）和佛波12-肉豆蔻酸酯13-乙酸酯（PMA）介导的ROS产生，测试人脐静脉内皮细胞（HUVEC）对中性粒细胞/单核细胞功能的影响，脱粒和白介素（IL）-8的产生。另外，测试了在存在或不存在HUVEC的情况下脂多糖（LPS）刺激的PBMC产生肿瘤坏死因子（TNF）-α的能力。 HUVEC被fMLP刺激的中性粒细胞剂量依赖性地抑制ROS的产生，但不影响脱粒。 HC和AAV的中性粒细胞之间未发现差异。但是，只有一名活动患者仅在接受环磷酰胺治疗之前被HUVEC显着抑制了脱粒，但在6周后没有。 HUVEC与LPS刺激的中性粒细胞/单核细胞的共培养可增加IL-8的产生，而TNF-α的产生则受到显着抑制。在这方面，AAV患者和HC之间无明显差异。我们的发现表明，HUVEC在刺激嗜中性粒细胞或单核细胞后能够抑制ROS并调节细胞因子的产生。我们的数据不支持内皮细胞不能充分抑制AAV患者中性粒细胞的ROS产生的假设。活跃患者可能存在中性粒细胞脱粒受损，但这一发现有待证实。

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