Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent
Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent
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DOI：
10.1006/taap.1997.8254
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发表时间：
1997-10-01
影响因子：
3.8
通讯作者：
Devlin, RB
中科院分区：
文献类型：
--
作者：
Carter, JD;Ghio, AJ;Devlin, RB
尽管许多流行病学研究支持环境空气污染颗粒物对人类健康有不利影响的论点，但对于能够解释与接触小于10 μ m的颗粒物有关的急性死亡率和发病率的生物学上合理的机制，还没有明确的一致意见。我们检验了空气污染颗粒中存在的金属可以诱导炎性细胞因子IL-8、IL-6和TNF α的合成和表达的假设。以含钒、镍、铁等过渡金属元素的渣油飞灰（ROFA）为模型排放源，研究了其对大气污染物颗粒物的影响。将正常人支气管上皮（NHBE）细胞暴露于0、5、50或200 μ g/ml ROFA 2或24小时。用市售ELISA试剂盒测量IL-8、IL-6和TNF-α蛋白的浓度。通过RT-PCR定量这些相同细胞因子的mRNA。暴露于ROFA的NHBE细胞产生大量的IL-8、IL-6和TNF，以及编码这些细胞因子的mRNA。通过包含金属螯合剂去铁胺（1.0 mM）或自由基清除剂二甲基硫脲（1.0 mM）抑制细胞因子的产生。此外，含钒化合物，但不是铁或镍硫酸盐，模仿完整的ROFA的影响。这些结果表明，ROFA中存在的金属可能是负责呼吸道上皮细胞的炎症介质的产生和释放，并表明这些介质可能有助于在流行病学研究中报告的颗粒空气污染物的毒性作用。(C)北京：科学出版社.
Despite the many epidemiological studies supporting the contention that ambient air pollution particles can adversely affect human health, there is no clear agreement as to a biologically plausible mechanism which can explain the acute mortality and morbidity associated with exposure to particles less than 10 mu m in size. We tested the hypothesis that metals present in an air pollution particle can induce the synthesis and expression of the inflammatory cytokines IL-8, IL-6, and TNF alpha. A residual oil fly ash (ROFA) containing the transition metals vanadium, nickel, and iron was used as a model emission source air pollution particle. Normal human bronchial epithelial (NHBE) cells were exposed for either 2 or 24 hr to 0, 5, 50, or 200 mu g/ml ROFA. Concentrations of IL-8, IL-6, and TNF-alpha proteins were measured with commercially available ELISA kits. mRNA for these same cytokines was quantified by RT-PCR. NHBE cells exposed to ROFA produced significant amounts of IL-8, IL-6, and TNF, as well as mRNAs coding for these cytokines. Cytokine production was inhibited by the inclusion of either the metal chelator deferoxamine (1.0 mM) or the free radical scavenger dimethylthiourea (1.0 mM). In addition, vanadium containing compounds, but not iron or nickel sulfates, mimicked the effects of intact ROFA. These results demonstrate that metals present in ROFA may be responsible for production and release of inflammatory mediators by the respiratory tract epithelium and suggest that these mediators may contribute to the toxic effects of particulate air pollutants reported in epidemiology studies. (C) 1997 Academic Press.