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Artemisia Pollen Extracts Exposed to Diesel Exhaust Enhance Airway Inflammation and Immunological Imbalance in Asthmatic Mice Model

机译:艾蒿属花粉提取物暴露于柴油排气,增强哮喘小鼠模型中的气道炎症和免疫不平衡

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Background: Vehicle-induced air pollution may increase the prevalence and severity of asthma. Pollens are important sources of outdoor allergens associated with asthma. Outdoor pollution may influence the structure of pollen grains, resulting in enhanced immune reactions. Objective: This study aims to investigate the impact that artemisia pollen extracts exposed to diesel emissions (APEDE) may induce - allergic airway inflammation, pulmonary pathology and immune imbalance - in mice. Methods: Sixty male Balb/c mice were equally randomized into 5 groups, sensitized with 30 mu L artemisia pollen extracts (APE) or APEDE adsorbed on 2 mg aluminum hydroxide gel by intraperitoneal injection on day 0, 7, 14, and 22, and challenged intranasally once per day with 30 mu L APE or APEDE from day 29 to 36. The controlling group used phosphate-buffered saline as control. Results: In mice immunized and challenged by APEDE, the clinical phenotype of eosinophils, neutrophils in bronchoalveolar lavage fluid (BALF), tracheal wall thickness, airway smooth muscle thickness and airway resistance increased significantly. Pathophysiological parameters such as interleukin (IL)-17A and tumour necrosis factor-alpha production in BALF and serum, and the ratio of Th17/Treg cells in CD4(+) cells increased significantly, while IL-10 in BALF and serum and the ratio of Treg cells decreased significantly. It was further found that the expression of oxidative stress marker 3-nitrotyrosine (3-NT) and the activation of nuclear factor kappa B (NF-kappa B) were significantly increased. The correlation analysis showed that the expression of 3-NT was positively correlated with the activation of NF-kappa B. Conclusion: Our findings suggested that pollens exposed to diesel exhaust enhance allergic responses, which may contribute to an increased prevalence of allergic diseases in urban environments with serious exhaust emissions.
机译:背景:车辆诱导的空气污染可能会增加哮喘的患病率和严重程度。花粉是与哮喘相关的户外过敏原的重要来源。户外污染可能影响花粉颗粒的结构,导致免疫反应增强。目的:本研究旨在探讨暴露于柴油排放(APEDE)的蒿属植物花粉提取物的影响可能会诱导 - 过敏气道炎症,肺病病理和免疫不平衡 - 在小鼠中。方法:60只雄性BALB / C小鼠同样随机随机分为5组,用30μlARTEMISIA花粉提取物(APE)或在第0天,7,14和22天通过腹腔注射吸附在2mg氢氧化铝凝胶上的α或α每天患上一次患有30亩的患者或者在第29天至36天中挑战一次。控制组使用磷酸盐缓冲盐水作为对照。结果:嗜血栓血液粒细胞患者临床表型,嗜酸性粒细胞灌洗液(BALF),气道厚度,气道平滑肌厚度和气道阻力大大明显增加了嗜酸性粒细胞的临床表型。在BALF和血清中的白细胞介素(IL)-17A和肿瘤坏死因子-α产生的病理生理学参数,以及CD4(+)细胞中的TH17 / Treg细胞的比例显着增加,而BALF和血清中的IL-10和比例Treg细胞显着下降。进一步发现,氧化应激标记物3-硝基霉素(3-NT)的表达和核因子Kappa B(NF-Kappa B)的活化明显增加。相关分析表明,3-NT的表达与NF-κB的活化呈正相关。结论:我们的研究结果表明,暴露于柴油排气的花粉增强过敏反应,这可能导致城市过敏性疾病的患病率增加增加有严重排放的环境。

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