Outdoor air pollution exposure increases chronic obstructive pulmonary disease (COPD) hospitalisations, and may contribute to COPD development. The mechanisms of harm, and the extent to which at-risk populations are more susceptible are not fully understood. Neutrophils are recruited to the lung following diesel exhaust exposure, a model of traffic-related air pollution (TRAP), but their functional role in this response is unknown. The purpose of this controlled human-exposure crossover study was to assess the effects of acute diesel exhaust exposure on neutrophil function in never-smokers and at-risk populations, with support from additional in vitro studies. 18 participants, including never-smokers (n=7), ex-smokers (n=4) and mild–moderate COPD patients (n=7), were exposed to diesel exhaust and filtered air for 2 h on separate occasions, and neutrophil function in blood (0 h and 24 h post-exposure) and bronchoalveolar lavage (24 h post-exposure) was assessed. Compared to filtered air, diesel exhaust exposure reduced the proportion of circulating band cells at 0 h, which was exaggerated in COPD patients. Diesel exhaust exposure increased the amount of neutrophil extracellular traps (NETs) in the lung across participants. COPD patients had increased peripheral neutrophil activation following diesel exhaust exposure. In vitro, suspended diesel exhaust particles increased the amount of NETs measured in isolated neutrophils. We propose NET formation as a possible mechanism through which TRAP exposure affects airway pathophysiology. In addition, COPD patients may be more prone to an activated inflammatory state following exposure. This is the first controlled human TRAP exposure study directly comparing at-risk phenotypes (COPD and ex-smokers) with lower-risk (never-smokers) participants, elucidating the human susceptibility spectrum. Acute human exposure to traffic-related air pollution leads lower airway neutrophils to release neutrophil extracellular traps, linked to COPD severity and airflow limitation. Ex-smokers and COPD patients mount a greater neutrophil response to exposure. http://bit.ly/2DEsYzE

中文翻译：

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急性空气污染暴露会改变从不吸烟者和高危人群的中性粒细胞

室外空气污染暴露会增加慢性阻塞性肺疾病 (COPD) 的住院率，并可能导致 COPD 的发展。伤害机制以及高危人群更容易受到影响的程度尚不完全清楚。中性粒细胞在柴油机尾气暴露后被募集到肺部，这是一种交通相关空气污染 (TRAP) 模型，但它们在这种反应中的功能作用尚不清楚。这项受控的人体暴露交叉​​研究的目的是在额外的体外研究的支持下，评估急性柴油机尾气暴露对从不吸烟者和高危人群中性粒细胞功能的影响。18 名参与者，包括从不吸烟者 (n=7)、戒烟者 (n=4) 和轻度至中度 COPD 患者 (n=7)，在不同的场合暴露于柴油机尾气和过滤空气中 2 小时，评估了血液（暴露后 0 小时和 24 小时）和支气管肺泡灌洗液（暴露后 24 小时）中的中性粒细胞功能。与过滤后的空气相比，柴油机尾气暴露降低了 0 小时时循环带状细胞的比例，这在 COPD 患者中被夸大了。柴油机尾气暴露增加了参与者肺部中性粒细胞胞外陷阱 (NET) 的数量。COPD 患者在柴油机尾气暴露后外周中性粒细胞活化增加。在体外，悬浮的柴油机尾气颗粒增加了在孤立的中性粒细胞中测量的 NETs 的数量。我们建议将 NET 形成作为 TRAP 暴露影响气道病理生理学的一种可能机制。此外，COPD 患者在暴露后可能更容易出现激活的炎症状态。这是第一个直接比较高风险表型（COPD 和戒烟者）与低风险（不吸烟者）参与者的受控人类 TRAP 暴露研究，阐明了人类易感性谱。人类急性暴露于交通相关的空气污染导致下呼吸道中性粒细胞释放中性粒细胞胞外陷阱，这与 COPD 的严重程度和气流受限有关。戒烟者和 COPD 患者对暴露的中性粒细胞反应更大。http://bit.ly/2DEsYzE 戒烟者和 COPD 患者对暴露的中性粒细胞反应更大。http://bit.ly/2DEsYzE 戒烟者和 COPD 患者对暴露的中性粒细胞反应更大。http://bit.ly/2DEsYzE