Department of Geriatrics, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Department of Respiratory, Shanghai General Hospital, Shanghai, China.
Int Arch Allergy Immunol. 2020;181(5):342-352. doi: 10.1159/000505747. Epub 2020 Feb 14.
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.
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.
Sixty male Balb/c mice were equally randomized into 5 groups, sensitized with 30 μL 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 μL APE or APEDE from day 29 to 36. The controlling group used phosphate-buffered saline as control.
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-α 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-κB) were significantly increased. The correlation analysis showed that the expression of 3-NT was positively correlated with the activation of NF-κB.
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.
车辆引起的空气污染可能会增加哮喘的发病率和严重程度。花粉是与哮喘相关的重要室外过敏原来源。室外污染可能会影响花粉粒的结构,导致免疫反应增强。
本研究旨在探讨受柴油排放物影响的青蒿花粉提取物(APEDE)可能在小鼠中引起的过敏气道炎症、肺部病理和免疫失衡的影响。
将 60 只雄性 Balb/c 小鼠随机均分为 5 组,通过腹腔注射 30 μL 青蒿花粉提取物(APE)或 APEDE 吸附在 2 mg 氢氧化铝凝胶上,于第 0、7、14 和 22 天进行致敏,然后于第 29 至 36 天每天通过鼻腔内挑战 30 μL APE 或 APEDE。对照组使用磷酸盐缓冲盐水作为对照。
在接受 APEDE 免疫和挑战的小鼠中,支气管肺泡灌洗液(BALF)中嗜酸性粒细胞和中性粒细胞的临床表型、气管壁厚度、气道平滑肌厚度和气道阻力显著增加。BALF 和血清中白细胞介素(IL)-17A 和肿瘤坏死因子-α的产生以及 CD4+细胞中 Th17/Treg 细胞的比值等病理生理参数显著增加,而 BALF 和血清中的 IL-10 和 Treg 细胞的比值显著降低。进一步发现,氧化应激标志物 3-硝基酪氨酸(3-NT)的表达和核因子 kappa B(NF-κB)的激活显著增加。相关性分析表明,3-NT 的表达与 NF-κB 的激活呈正相关。
我们的研究结果表明,暴露于柴油尾气的花粉增强了过敏反应,这可能导致在严重尾气排放的城市环境中过敏疾病的发病率增加。