臭氧能诱导支气管上皮细胞炎症
2010/12/29
摘要
目的：臭氧是汽车尾气二次污染物的主要组成成分。城市儿童臭氧暴露可能与哮喘的发生相关。然而，有关臭氧对人体气道上皮细胞和随后的气道炎症的影响及其机制了解较少。
方法：人支气管上皮细胞暴露于0.16 mg/m3的臭氧下不同的时间。采用ELISA方法检测细胞分泌的IL-1和IL-6含量，同时检测细胞内丙二醛（MDA）的含量。此外，将臭氧暴露后的细胞条件培养液，用于刺激来自于哮喘患者和健康个体的外周T淋巴细胞，采用ELISA和实时定量PCR(RT-PCR)检测细胞因子含量。
结果：臭氧能刺激BEAS-2B细胞产生IL-1和IL-6，该刺激作用呈现时间依赖性。此外，与无臭氧暴露的细胞相比，臭氧暴露能显著增加BEAS-2B细胞内MDA含量，该作用同样存在暴露时间依赖性。臭氧暴露后的细胞条件培养液能显著增加哮喘患者，而非正常个体，外周T淋巴细胞IL-1 mRNA的产生。而该条件培养液却不能诱导IL-2的产生。
结论：我们的结果显示，短期低水平的臭氧暴露，能增加上皮细胞促炎标志物的产生和氧化应激，从而导致气道炎症，特别是在哮喘患儿中。
（苏楠 审校）
J Asthma. 2010 Nov 3. [Epub ahead of print]
Ozone Induces Inflammation in Bronchial Epithelial Cells.
Song H, Tan W, Zhang X.
Department of Preventive Medicine, School of Public Health, Sun Yat-Sen University, GuangzhouP.R. China.
Abstract
Aim. Ozone is a main component of secondary pollutants of vehicle exhausts, and ozone exposure to children in urban areas may be associated with the development of asthma. However, little is known about the mechanism(s) by which ozone affects human airway epithelium and subsequent airway inflammation.
Methods. Human bronchial epithelial cells were exposed to ozone at 0.16 mg/m(3) for varying periods. The concentrations of IL-1 and IL-6 secreted by the cells were measured by enzyme-linked immunosorbent assay (ELISA) and the contents of intracellular malondialdehyde (MDA) were determined. Furthermore, the conditional medium from the ozone-exposed cells was examined for stimulating human peripheral T lymphocytes from asthmatic patients and healthy subjects, and the production of cytokines was characterized by ELISA and quantitative real-time polymerase chain reaction (RT-PCR).
Results. Ozone stimulated the IL-1 and IL-6 production by BEAS-2B cells and its stimulatory effects were time dependent. Furthermore, ozone exposure significantly increased the levels of MDA in BEAS-2B cells, as compared with that of the cells without ozone exposure, in a time-dependent manner. In addition, the conditional medium from the cells exposed to ozone, but not control condition medium, significantly increased the relative levels of IL-1 mRNA transcripts in human peripheral T lymphocytes from asthmatic patients, but not healthy subjects. However, the conditional medium did not induce significantly increased levels of IL-2 production by peripheral T cells.
Conclusions. Our data indicated that exposure to low levels of ozone for a short period induced increases in the pro-inflammatory markers and oxidative stress in epithelial cells, which might contribute to airway inflammation particularly in asthmatic children.
J Asthma. 2010 Nov 3. [Epub ahead of print]
目的：臭氧是汽车尾气二次污染物的主要组成成分。城市儿童臭氧暴露可能与哮喘的发生相关。然而，有关臭氧对人体气道上皮细胞和随后的气道炎症的影响及其机制了解较少。
方法：人支气管上皮细胞暴露于0.16 mg/m3的臭氧下不同的时间。采用ELISA方法检测细胞分泌的IL-1和IL-6含量，同时检测细胞内丙二醛（MDA）的含量。此外，将臭氧暴露后的细胞条件培养液，用于刺激来自于哮喘患者和健康个体的外周T淋巴细胞，采用ELISA和实时定量PCR(RT-PCR)检测细胞因子含量。
结果：臭氧能刺激BEAS-2B细胞产生IL-1和IL-6，该刺激作用呈现时间依赖性。此外，与无臭氧暴露的细胞相比，臭氧暴露能显著增加BEAS-2B细胞内MDA含量，该作用同样存在暴露时间依赖性。臭氧暴露后的细胞条件培养液能显著增加哮喘患者，而非正常个体，外周T淋巴细胞IL-1 mRNA的产生。而该条件培养液却不能诱导IL-2的产生。
结论：我们的结果显示，短期低水平的臭氧暴露，能增加上皮细胞促炎标志物的产生和氧化应激，从而导致气道炎症，特别是在哮喘患儿中。
（苏楠 审校）
J Asthma. 2010 Nov 3. [Epub ahead of print]
Ozone Induces Inflammation in Bronchial Epithelial Cells.
Song H, Tan W, Zhang X.
Department of Preventive Medicine, School of Public Health, Sun Yat-Sen University, GuangzhouP.R. China.
Abstract
Aim. Ozone is a main component of secondary pollutants of vehicle exhausts, and ozone exposure to children in urban areas may be associated with the development of asthma. However, little is known about the mechanism(s) by which ozone affects human airway epithelium and subsequent airway inflammation.
Methods. Human bronchial epithelial cells were exposed to ozone at 0.16 mg/m(3) for varying periods. The concentrations of IL-1 and IL-6 secreted by the cells were measured by enzyme-linked immunosorbent assay (ELISA) and the contents of intracellular malondialdehyde (MDA) were determined. Furthermore, the conditional medium from the ozone-exposed cells was examined for stimulating human peripheral T lymphocytes from asthmatic patients and healthy subjects, and the production of cytokines was characterized by ELISA and quantitative real-time polymerase chain reaction (RT-PCR).
Results. Ozone stimulated the IL-1 and IL-6 production by BEAS-2B cells and its stimulatory effects were time dependent. Furthermore, ozone exposure significantly increased the levels of MDA in BEAS-2B cells, as compared with that of the cells without ozone exposure, in a time-dependent manner. In addition, the conditional medium from the cells exposed to ozone, but not control condition medium, significantly increased the relative levels of IL-1 mRNA transcripts in human peripheral T lymphocytes from asthmatic patients, but not healthy subjects. However, the conditional medium did not induce significantly increased levels of IL-2 production by peripheral T cells.
Conclusions. Our data indicated that exposure to low levels of ozone for a short period induced increases in the pro-inflammatory markers and oxidative stress in epithelial cells, which might contribute to airway inflammation particularly in asthmatic children.
J Asthma. 2010 Nov 3. [Epub ahead of print]
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血清免疫球蛋白水平作为儿童非过敏性哮喘预后较好的一个预测指标
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哮喘患者红细胞膜鞘磷脂代谢
