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首页> 外文期刊>International archives of allergy and immunology >The Proinflammatory Potential of Nitrogen Dioxide and Its Influence on the House Dust Mite Allergen Der p 1
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The Proinflammatory Potential of Nitrogen Dioxide and Its Influence on the House Dust Mite Allergen Der p 1

机译:二氧化氮的促炎潜力及其对屋尘螨变应原Der p 1的影响

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摘要

Asthma and allergies are both major global health problems with an increasing prevalence, and environmental data implicate an influence of air pollutants on their development. The present study focuses on the influence of nitrogen dioxide (NO2) and the major allergen of the house dust mite Der p 1 on human nasal epithelial cells of nonallergic patients in vitro. Nasal epithelial mucosa samples of 11 donors were harvested during nasal air passage surgery and cultured as an air-liquid interface. Exposure to 0.1, 1 and 10 ppm NO2 or synthetic air as a control was performed for 1 h. Subsequently, the cells were exposed to Der p 1 for 24 h. The release of interleukin (IL)-6 and IL-8 was measured by ELISA, and the production of IL-6 mRNA and IL-8 mRNA was measured by RT-PCR. NO2 exposure resulted in a concentration-dependent release of IL-6, but not IL-8 release. The coexposure of 0.1 ppm NO2 and Der p 1, or 1 ppm NO2 and Der p 1 significantly increased both IL-6 and IL-8 release. Exposure to NO2, Der p 1, or their combination, did not significantly influence the production of IL-6 or IL-8 mRNA. In conclusion, NO2 in-creases the release of inflammatory cytokines in human nasal epithelial cells, especially in coexposure with Der p 1, as a mechanism of allergotoxicology. (C) 2016 S. Karger AG, Basel
机译:哮喘和过敏症都是全球性的主要健康问题,患病率不断上升,环境数据暗示了空气污染物对其发展的影响。本研究的重点是二氧化氮(NO2)和屋尘螨Der p 1的主要过敏原对非过敏性病人的人鼻上皮细胞的体外影响。在鼻气道手术期间收集了11个供体的鼻上皮粘膜样品,并作为气液界面进行培养。暴露于0.1、1和10 ppm的NO2或作为对照的合成空气中暴露1小时。随后,将细胞暴露于Der p 1 24小时。通过ELISA测定白介素(IL)-6和IL-8的释放,通过RT-PCR测定IL-6mRNA和IL-8mRNA的产生。 NO2暴露导致浓度依赖性的IL-6释放,但不是IL-8释放。 0.1 ppm NO2和Der p 1或1 ppm NO2和Der p 1的共同暴露会显着增加IL-6和IL-8的释放。暴露于NO2,Der p 1或它们的组合不会显着影响IL-6或IL-8 mRNA的产生。总之,NO2增加了人鼻上皮细胞中炎性细胞因子的释放,特别是与Der p 1共同暴露时,作为变态反应毒理学的一种机制。 (C)2016 S.Karger AG,巴塞尔

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