Human airway epithelial cells in culture for studying the molecular mechanisms of the inflammatory response triggered by diesel exhaust particles
Human airway epithelial cells in culture for studying the molecular mechanisms of the inflammatory response triggered by diesel exhaust particles
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DOI：
10.1023/a:1019548517877
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发表时间：
2002-01-01
影响因子：
6.1
通讯作者：
Baeza-Squiban, A
中科院分区：
文献类型：
--
作者：
Marano, F;Boland, S;Baeza-Squiban, A
流行病学研究表明，颗粒性空气污染与呼吸道疾病的发病率和死亡率增加有关。柴油废气颗粒物(DEPS)是西欧和日本城市地区PM2.5的最重要组成部分，已被怀疑。用人上皮细胞系(16-HBE)研究了DEPS诱导炎症反应的机制。研究表明，DEPS可被HBE细胞吞噬，诱导细胞因子的释放。MAP激酶通路(即ERK1/2和P38)被触发，核因子NF-kappaB也被激活。由于DEPS诱导细胞内过氧化氢的增加，抗氧化剂抑制DEP诱导的细胞因子的释放、MAP激酶和核因子-kappaB的激活，因此这种反应与ROS密切相关。吸附在DEPS上的有机化合物似乎参与了ROS的反应和产生。此外，我们还证明了DEPS可以激活HBE细胞中的CYP1A1。这些实验结果为流行病学发现提供了生物学上的可信性。
Epidemiological studies have shown that particulate air pollution is linked to the increase of morbidity and mortality due to respiratory diseases. Diesel exhaust particles (DEPs), which are the most important part of PM2.5 in Western European and Japanese urban areas, have been suspected. The mechanisms of proinflammatory response induced by DEPS were elucidated using a human epithelial cell line (16-HBE). It has been shown that DEPs can be phagocytosed by HBE cells, inducing the release of cytokines. MAP kinase pathways (i.e., ERK1/2 and P38) were triggered as well as the activation of the nuclear factor NF-kappaB. Reactive oxygen species (ROS) were strongly incriminated in this response because DEPs induce the increase of intracellular hydroperoxides and antioxidants inhibit the release of DEP-induced cytokines, the activation of MAP kinases and NF-kappaB. Organic compounds adsorbed on DEPs seemed to be involved in the response and the production of ROS. Moreover, we have demonstrated that DEPs can activate CYP1A1 in HBE cells. These experimental results give biological plausibility to the epidemiological findings.