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暴露于柴油机排气微米亚颗粒(PM₁.₀)和花粉过敏原后对人肺上皮细胞的炎症作用。

Inflammatory effects on human lung epithelial cells after exposure to diesel exhaust micron sub particles (PM₁.₀) and pollen allergens.

机构信息

Department of Cardio-Thoracic and Respiratory Sciences, Second University of Naples, Italy.

出版信息

Environ Pollut. 2012 Feb;161:64-9. doi: 10.1016/j.envpol.2011.09.046. Epub 2011 Nov 2.

DOI:10.1016/j.envpol.2011.09.046
PMID:22230069
Abstract

Asthma is currently defined as a chronic inflammatory disease of the airway. Several evidence indicate that vehicle emissions in cities is correlated with the allergic respiratory diseases. In the present study, we evaluated in the A549 cells the production and release of IL-4, IL-5 and IL-13 after treatment with sub-micron PM(1.0) particles (PM(1.0)), Parietaria officinalis (ALL), and PM(1.0) + ALL together. Our data demonstrated that PM(1.0) + ALL together exhibited the greatest capacity to induce A549 cells to enhance the expression of IL-4 and IL-5 compared with the only PM(1.0) or ALL treatment. Interestingly, IL-13 that is necessary for allergen-induced airway hyper responsiveness, is increased in cells treated with PM(1.0) + ALL together, but is higher expressed when the cells are treated only with the allergen. Our data support the hypothesis that the urban environment damage the acinar lung units and activates cells of the immune system.

摘要

哮喘目前被定义为一种气道的慢性炎症性疾病。有几项证据表明,城市车辆排放物与过敏性呼吸道疾病有关。在本研究中,我们评估了亚微米 PM(1.0) 颗粒 (PM(1.0))、法国梧桐花粉 (ALL) 以及 PM(1.0) + ALL 共同处理后 A549 细胞中 IL-4、IL-5 和 IL-13 的产生和释放。我们的数据表明,与仅用 PM(1.0) 或 ALL 处理相比,PM(1.0) + ALL 共同处理表现出最大的能力诱导 A549 细胞增强 IL-4 和 IL-5 的表达。有趣的是,IL-13 是变应原诱导气道高反应性所必需的,在用 PM(1.0) + ALL 共同处理的细胞中增加,但在仅用变应原处理的细胞中表达更高。我们的数据支持这样一种假设,即城市环境破坏腺泡肺单位并激活免疫系统细胞。

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