Ohtoshi T, Takizawa H, Okazaki H, Kawasaki S, Takeuchi N, Ohta K, Ito K
Department of Medicine, University of Tokyo, School of Medicine, Japan.
J Allergy Clin Immunol. 1998 Jun;101(6 Pt 1):778-85. doi: 10.1016/S0091-6749(98)70307-0.
Epidemiologic and experimental studies suggest that air pollution such as diesel exhaust particles (DEPs), one of the important air pollutants, may play a role in the increasing prevalence of allergic airway diseases.
We studied the effect of suspended particulate matter (SPM) and its main component, DEPs, on the production of IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by human airway epithelial cells in vitro.
SPM obtained from high-volume air samplers and DEPs were added to cultured human nasal polyp-derived upper airway, normal bronchial, and transformed bronchial epithelial cells. Production of GM-CSF and IL-8 by airway epithelial cells was evaluated.
Nontoxic doses of DEPs showed a significant stimulatory effect on IL-8 and GM-CSF production by these three kinds of epithelial cells in a dose- and time-dependent fashion. SPM had a stimulatory effect on GM-CSF, but not IL-8, production. These effects were abrogated by treatment with a protein synthesis inhibitor, cycloheximide, suggesting that the process required a de novo protein synthesis. On the double-chamber plates, airway epithelial cells responded to DEPs only when they were stimulated from the apical sides, which can be a model for in vivo environments. Neither charcoal nor graphite showed such stimulatory effects, indicating that the activity of DEPs did not derive from their particulate nature. Benzo(a)pyrene, one of the main aromatic hydrocarbons contained in DEPs, showed a stimulatory effect on the release of the cytokines, and this organic substance might have a causative effect on of the potency of DEPs.
We conclude that SPM and DEPs, its main component, might be important air pollutants in the activation of airway epithelial cells for the release of cytokines relevant to allergic airway inflammation.
流行病学和实验研究表明，空气污染如柴油废气颗粒（DEPs），作为重要的空气污染物之一，可能在过敏性气道疾病患病率上升中起作用。
我们在体外研究了悬浮颗粒物（SPM）及其主要成分DEPs对人气道上皮细胞白细胞介素-8（IL-8）和粒细胞巨噬细胞集落刺激因子（GM-CSF）产生的影响。
将大容量空气采样器收集的SPM和DEPs添加到培养的源自人鼻息肉的上呼吸道、正常支气管和转化支气管上皮细胞中。评估气道上皮细胞GM-CSF和IL-8的产生。
无毒剂量的DEPs对这三种上皮细胞的IL-8和GM-CSF产生呈剂量和时间依赖性的显著刺激作用。SPM对GM-CSF产生有刺激作用，但对IL-8产生无刺激作用。用蛋白质合成抑制剂环己酰亚胺处理可消除这些作用，表明该过程需要从头合成蛋白质。在双室培养板上，气道上皮细胞仅在从顶端侧受到刺激时才对DEPs有反应，这可作为体内环境的模型。炭和石墨均未显示出这种刺激作用，表明DEPs的活性并非源于其颗粒性质。DEPs中含有的主要芳香烃之一苯并(a)芘对细胞因子的释放有刺激作用，这种有机物质可能对DEPs的效力有致病作用。
我们得出结论，SPM及其主要成分DEPs可能是激活气道上皮细胞释放与过敏性气道炎症相关细胞因子的重要空气污染物。
