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首页> 外文期刊>Occupational and environmental medicine >The procoagulant potential of environmental particles (PM10).
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The procoagulant potential of environmental particles (PM10).

机译：环境颗粒（PM10）的促凝潜力。

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BACKGROUND AND AIMS: Epidemiology studies have shown that cardiovascular (CV) disease is primarily responsible for the mortality associated with increased pulmonary environmental particle (PM10) exposure. The mechanisms involved in PM10 mediated CV effects are unknown although changes in plasma viscosity and in the homoeostasis of blood coagulation have been implicated. It was hypothesised that PM10 exposure would result in an inflammatory response and enhance the activation of the extrinsic coagulation mechanisms in pulmonary and vascular cells in culture. METHODS: Primary human monocyte derived macrophages and human umbilical cord vein endothelial, human alveolar type II epithelial (A549), and human bronchial epithelial (16HBE) cells were tested for their inflammatory and procoagulant response to PM10 exposure. IL-8, tissue factor (TF), and tissue plasminogen activator (tPA) gene expression and protein release, and coagulation enhancing ability of culture media were determined 6 and 24 hours following exposure. RESULTS: The culture media from macrophages and 16HBE bronchial epithelial cells, but not A549 cells, exposed to PM10 had an enhanced ability to cause clotting. Furthermore, H2O2 also increased the clotting activity. Apoptosis was significantly increased in macrophages exposed to PM10 and LPS as shown by annexin V binding. TF gene expression was enhanced in macrophages exposed to PM10, and HUVEC tissue factor and tPA gene and protein expression were inhibited. CONCLUSIONS: These data indicate that PM10 has the ability to alter macrophage, epithelial, and endothelial cell function to favour blood coagulation via activation of the extrinsic pathway and inhibition of fibrinolysis pathways.
机译：背景与目的：流行病学研究表明，心血管（CV）疾病是造成与增加的肺环境颗粒（PM10）暴露相关的死亡率的主要原因。尽管涉及血浆粘度的变化和血液凝固的均流，但参与PM10介导的CV效应的机制尚不清楚。假设PM10暴露会导致炎症反应并增强培养的肺和血管细胞内外凝血机制的激活。方法：检测原代人单核细胞衍生的巨噬细胞和人脐带静脉内皮，人肺泡II型上皮（A549）和人支气管上皮（16HBE）细胞对PM10暴露的炎症和促凝反应。暴露后6小时和24小时测定IL-8，组织因子（TF）和组织纤溶酶原激活物（tPA）基因表达和蛋白质释放以及培养基的增强凝结能力。结果：暴露于PM10的巨噬细胞和16HBE支气管上皮细胞培养基，而不是A549细胞，具有增强的凝血能力。此外，H2O2还增加了凝血活性。膜联蛋白V结合显示，暴露于PM10和LPS的巨噬细胞凋亡显着增加。暴露于PM10的巨噬细胞中TF基因表达增强，而HUVEC组织因子以及tPA基因和蛋白质表达受到抑制。结论：这些数据表明，PM10具有改变巨噬细胞，上皮和内皮细胞功能的能力，从而通过激活外在途径和抑制纤溶途径来促进血液凝结。

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