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Diesel exhaust particle and dust mite induced airway inflammation is modified by cerium dioxide nanoparticles

机译:二氧化铈纳米颗粒改善了柴油机排气颗粒和尘螨引起的气道炎症

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Cerium dioxide nanoparticles (CeO_2NPs) have been used as diesel fuel-borne catalysts for improved efficiency and pollutant emissions. Concerns that such material may influence diesel exhaust particle (DEP) effects within the lung upon inhalation, prompted us to examine particle responses in mice in the presence and absence of the common allergen house dust mite (HDM). Repeated intranasal instillation of combined HDM and DEP increased airway mucin, eosinophils, lymphocytes, IL-5, IL-13, IL-17A and plasma IgE, which were further increased with CeO_2NPs co-exposure. A single co-exposure of CeO_2NPs and DEP after repeated HDM exposure increased macrophage and IL-17A levels above DEP induced levels. CeO_2NPs exposure in the absence of HDM also resulted in increased levels of plasma IgE and airway mucin staining, changes not observed with repeated DEP exposure alone. These observations indicate that CeO_2NPs can modify exhaust particulate and allergen induced inflammatory events in the lung with the potential to influence conditions such as allergic airway disease.
机译:二氧化铈纳米颗粒(CeO_2NPs)已用作柴油燃料催化剂,以提高效率和污染物排放。由于担心这种物质可能会影响吸入后肺内的柴油机废气颗粒(DEP)效果,促使我们在有和没有普通过敏原尘螨(HDM)的情况下检查小鼠的颗粒反应。重复鼻内滴注HDM和DEP会增加气道粘蛋白,嗜酸性粒细胞,淋巴细胞,IL-5,IL-13,IL-17A和血浆IgE,并随着CeO_2NPs共同暴露而进一步增加。反复暴露于HDM后,一次CeO_2NPs和DEP共同暴露会使巨噬细胞和IL-17A水平高于DEP诱导水平。在不存在HDM的情况下,暴露于CeO_2NPs也会导致血浆IgE水平升高和气道粘蛋白染色,仅通过重复DEP暴露就无法观察到这种变化。这些观察结果表明,CeO_2NPs可以修饰排气中的微粒和变应原诱发的肺部炎症事件,并可能影响诸如变应性气道疾病等疾病。

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