Indirect effect of PM1 on endothelial cells via inducing the release of respiratory inflammatory cytokines
Indirect effect of PM1 on endothelial cells via inducing the release of respiratory inflammatory cytokines
复制标题
PM1通过诱导呼吸道炎症细胞因子的释放对内皮细胞产生间接影响
DOI：
10.1016/j.tiv.2019.03.013
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发表时间：
2019-06-01
影响因子：
3.2
通讯作者：
Zhang, Fang
中科院分区：
文献类型：
--
作者：
Tian, Guoxiong;Wang, Juan;Zhang, Fang
大量流行病学研究表明，心血管病发病率和死亡率的增加与暴露于高浓度的PM2.5有关。PM2.5影响心血管系统的方式之一是通过全身炎症。炎性细胞因子如TNF-α、IL-1 β、IL-6和IL-8刺激内皮细胞，这导致内皮功能障碍。与PM2.5相比，PM 1的尺寸更小，表面积更大，吸收更多的有毒物质，如重金属，有机化合物和黑碳。然而，PM 1对人体健康的影响研究较少。在这里，我们使用BEAS-2B细胞和分化的THP-1细胞分别模拟肺中的上皮细胞和巨噬细胞。用共培养模型研究了PM 1对内皮细胞的间接作用，该模型由transwell板的顶室中的两个细胞系（BEAS-2B细胞和巨噬细胞）和底室中的一个细胞系（人脐静脉内皮细胞（EA.hy926））组成。结果表明，PM 1可促进BEAS 2B细胞和巨噬细胞释放TNF-α和IL-6等炎性细胞因子。此外，PM 1通过TNF-α/NF-κ B信号通路上调EA.hy926细胞中ICAM-1的表达，促进内皮细胞和单核细胞的粘附，这是动脉粥样硬化起始的关键事件。
A large number of epidemiological studies have shown that increased cardiovascular morbidity and mortality are associated with exposure to high concentrations of PM2.5. One of the ways that PM2.5 affects the cardiovascular system is through systemic inflammation. Inflammatory cytokines such as TNF-alpha, IL-1 beta, IL-6 and IL-8 stimulate endothelial cells, which leads to endothelial dysfunction. Compared with PM2.5, PM1 is smaller in size, has a larger surface area and absorbs more toxic substances such as heavy metals, organic compounds, and black carbon. However, the effect of PM1 on human health is less studied. Here, we used BEAS-2B cells and differentiated THP-1 cells to simulate epithelial cells and macrophages in the lung, respectively. The indirect effect of PM1 on endothelial cells was studied with a coculture model consisting of two cell lines (BEAS-2B cells and macrophages) in the top compartment and one cell line, human umbilical vein endothelial cells (EA.hy926), in the bottom compartment of a transwell plate. The results showed that PM 1 could promote the release of inflammatory cytokines, including TNF-alpha and IL-6, from BEAS-2B cells and macrophages. In addition, PM1 up-regulated ICAM-1 expression in EA.hy926 cells through TNF-alpha/NF-kappa B signaling pathways, promoting the adhesion of endothelial cells and monocytes, a key event in the initiation of atherosclerosis.