Proinflammatory effects and oxidative stress within human bronchial epithelial cells exposed to atmospheric particulate matter (PM2.5 and PM>2.5) collected from Cotonou, Benin
Proinflammatory effects and oxidative stress within human bronchial epithelial cells exposed to atmospheric particulate matter (PM2.5 and PM>2.5) collected from Cotonou, Benin
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DOI：
10.1016/j.envpol.2013.10.026
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发表时间：
2014-02-01
影响因子：
8.9
通讯作者：
Shirali, Pirouz
中科院分区：
文献类型：
--
作者：
Cachon, Boris Fresnel;Firmin, Stephane;Shirali, Pirouz
在科托努（贝宁）收集颗粒物（PM）后，对PM 2.5和PM>2.5进行了完整的理化表征。然后，通过体外培养人肺细胞来评估它们的不良健康影响。BEAS-2B（支气管上皮细胞）在增加PM浓度（1.5-96 μ g/cm（2））的短期暴露期间中毒，以确定总体细胞毒性。因此，将细胞暴露于3和12 μ g/cm（2），以研究PM毒性产生的潜在生物失衡。我们的研究结果表明，PM诱导氧化应激和引起炎症细胞因子/趋化因子基因表达和分泌的能力。此外，PM能够诱导参与异生物质代谢途径的酶的基因表达。发现代谢酶的基因表达、促炎反应和细胞周期改变之间以及促炎反应和细胞活力之间存在强相关性。应激氧化指标与炎症介质的表达和蛋白分泌高度相关。(C)2013爱思唯尔有限公司保留所有权利。
After particulate matter (PM) collection in Cotonou (Benin), a complete physicochemical characterization of PM2.5 and PM>2.5 was led. Then, their adverse health effects were evaluated by using in vitro culture of human lung cells. BEAS-2B (bronchial epithelial cells) were intoxicated during short-term exposure at increasing PM concentrations (1.5-96 mu g/cm(2)) to determine global cytotoxicity. Hence, cells were exposed to 3 and 12 mu g/cm(2) to investigate the potential biological imbalance generated by PM toxicity. Our findings showed the ability of both PM to induce oxidative stress and to cause inflammatory cytokines/chemokines gene expression and secretion. Furthermore, PM were able to induce gene expression of enzymes involved in the xenobiotic metabolism pathway. Strong correlations between gene expression of metabolizing enzymes, proinflammatory responses and cell cycle alteration were found, as well as between proinflammatory responses and cell viability. Stress oxidant parameters were highly correlated with expression and protein secretion of inflammatory mediators. (C) 2013 Elsevier Ltd. All rights reserved.