Song Hong, Tan Weipin, Zhang Xuchao
Department of Preventive Medicine, School of Public Health, Sun Yat-Sen University, Guangzhou, P.R. China.
J Asthma. 2011 Feb;48(1):79-83. doi: 10.3109/02770903.2010.529224. Epub 2010 Nov 3.
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.
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).
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.
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.
臭氧是汽车尾气二次污染物的主要成分，城市地区儿童接触臭氧可能与哮喘的发生有关。然而，关于臭氧影响人类气道上皮及随后气道炎症的机制知之甚少。
将人支气管上皮细胞暴露于0.16 mg/m³的臭氧中不同时间。通过酶联免疫吸附测定（ELISA）检测细胞分泌的白细胞介素-1（IL-1）和白细胞介素-6（IL-6）浓度，并测定细胞内丙二醛（MDA）含量。此外，检测暴露于臭氧的细胞的条件培养基对哮喘患者和健康受试者的人外周血T淋巴细胞的刺激作用，并通过ELISA和定量实时聚合酶链反应（RT-PCR）对细胞因子的产生进行表征。
臭氧刺激BEAS-2B细胞产生IL-1和IL-6，其刺激作用具有时间依赖性。此外，与未暴露于臭氧的细胞相比，臭氧暴露以时间依赖性方式显著增加了BEAS-2B细胞中MDA的水平。此外，暴露于臭氧的细胞的条件培养基而非对照条件培养基显著增加了哮喘患者而非健康受试者的人外周血T淋巴细胞中IL-1 mRNA转录本的相对水平。然而，条件培养基并未诱导外周血T细胞产生的IL-2水平显著增加。
我们的数据表明，短期暴露于低水平臭氧会导致上皮细胞中促炎标志物增加和氧化应激，这可能导致气道炎症，尤其是在哮喘儿童中。
