Differences in cytotoxicity versus pro-inflammatory potency of different PM fractions in human epithelial lung cells
Differences in cytotoxicity versus pro-inflammatory potency of different PM fractions in human epithelial lung cells
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DOI：
10.1016/j.tiv.2009.09.013
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发表时间：
2010-02-01
影响因子：
3.2
通讯作者：
Camatini, Marina
中科院分区：
文献类型：
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作者：
Gualtieri, Maurizio;Ovrevik, Johan;Camatini, Marina
由于颗粒物（PM10和PM2.5）浓度高，米兰的空气污染引起了健康问题。本研究的目的是探讨PM10和PM2.5化学成分的季节性差异及其对促炎细胞因子释放和细胞毒性的生物学效应。PM在冬季和夏季取样。冬季样品的多环芳烃含量高于夏季样品，而夏季样品含有较多的矿物粉尘元素。研究了PM对人肺上皮细胞株BEAS-2B和A549的毒性作用。通过ELISA检测，冬季PM10比夏季PM10具有更高的细胞毒性，而夏季PM10具有更高的促炎潜能。这种炎症潜能似乎部分是由于生物成分，如细菌脂多糖（LPS），通过使用Polymixin b进行评估。有趣的是，在BEAS-2B细胞中，冬季PM2.5由于有丝分裂延迟/停止而减少了增殖，而在A549细胞中没有观察到这种影响。这些结果强调，体外对PM的反应可能是细胞系依赖的，并表明PM的不同性质可能引发不同的终点，如炎症、细胞周期扰动和细胞死亡。2009爱思唯尔有限公司版权所有。
Air pollution in Milan causes health concern due to the high concentrations of particulate matter (PM10 and PM2.5). The aim of this study was to investigate possible seasonal differences in PM10 and PM2.5 chemical composition and their biological effects on pro-inflammatory cytokine release and cytotoxicity. The PM was sampled during winter and summer seasons. The winter PMs had higher levels of PAHs than the summer samples which contained a greater amount of mineral dust elements. The PM toxicity was tested in the human pulmonary epithelial cell lines BEAS-2B and A549. The winter PMs were more cytotoxic than summer samples, whereas the summer PM10 exhibited a higher pro-inflammatory potential, as measured by ELISA. This inflammatory potential seemed partly due to biological components such as bacterial lipopolysaccharides (LPS), as evaluated by the use of Polymixin B. Interestingly, in the BEAS-2B cells the winter PM2.5 reduced proliferation due to a mitotic delay/arrest, while no such effects were observed in the A549 cells. These results underline that the in vitro responsiveness to PM may be cell line dependent and suggest that the PM different properties may trigger different endpoints such as inflammation, perturbation of cell cycle and cell death. (C) 2009 Elsevier Ltd. All rights reserved.