Department of Medical Biochemistry and Biophysics, Division of Physiological Chemistry II, Karolinska Institutet, Stockholm, Sweden.
PLoS One. 2011;6(8):e23864. doi: 10.1371/journal.pone.0023864. Epub 2011 Aug 29.
Asthma is a chronic inflammatory lung disease that causes significant morbidity and mortality worldwide. Air pollutants such as particulate matter (PM) and oxidants are important factors in causing exacerbations in asthmatics, and the source and composition of pollutants greatly affects pathological implications.
This randomized crossover study investigated responses of the respiratory system to Stockholm subway air in asthmatics and healthy individuals. Eicosanoids and other oxylipins were quantified in the distal lung to provide a measure of shifts in lipid mediators in association with exposure to subway air relative to ambient air.
Sixty-four oxylipins representing the cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P450 (CYP) metabolic pathways were screened using liquid chromatography-tandem mass spectrometry (LC-MS/MS) of bronchoalveolar lavage (BAL)-fluid. Validations through immunocytochemistry staining of BAL-cells were performed for 15-LOX-1, COX-1, COX-2 and peroxisome proliferator-activated receptor gamma (PPARγ). Multivariate statistics were employed to interrogate acquired oxylipin and immunocytochemistry data in combination with patient clinical information.
Asthmatics and healthy individuals exhibited divergent oxylipin profiles following exposure to ambient and subway air. Significant changes were observed in 8 metabolites of linoleic- and α-linolenic acid synthesized via the 15-LOX pathway, and of the COX product prostaglandin E(2) (PGE(2)). Oxylipin levels were increased in healthy individuals following exposure to subway air, whereas asthmatics evidenced decreases or no change.
Several of the altered oxylipins have known or suspected bronchoprotective or anti-inflammatory effects, suggesting a possible reduced anti-inflammatory response in asthmatics following exposure to subway air. These observations may have ramifications for sensitive subpopulations in urban areas.
哮喘是一种慢性炎症性肺部疾病,在全球范围内造成了很高的发病率和死亡率。空气污染物,如颗粒物(PM)和氧化剂,是导致哮喘发作的重要因素,而污染物的来源和成分对病理影响有很大影响。
本随机交叉研究调查了呼吸系统对斯德哥尔摩地铁空气的反应,研究对象为哮喘患者和健康个体。在远端肺部中定量了类二十烷酸和其他氧化脂类,以提供与暴露于地铁空气相对于环境空气相关的脂质介质变化的衡量标准。
使用液相色谱-串联质谱法(LC-MS/MS)对支气管肺泡灌洗液(BAL)进行了 64 种氧化脂类的筛选,这些氧化脂类代表了环氧化酶(COX)、脂氧合酶(LOX)和细胞色素 P450(CYP)代谢途径。通过 BAL 细胞的免疫细胞化学染色对 15-LOX-1、COX-1、COX-2 和过氧化物酶体增殖物激活受体γ(PPARγ)进行了验证。采用多元统计方法结合患者临床信息来研究获得的氧化脂类和免疫细胞化学数据。
哮喘患者和健康个体在暴露于环境和地铁空气后表现出不同的氧化脂类谱。在通过 15-LOX 途径合成的亚油酸和α-亚麻酸的 8 种代谢物以及 COX 产物前列腺素 E2(PGE2)中观察到显著变化。健康个体暴露于地铁空气后,氧化脂类水平升高,而哮喘患者则表现出降低或无变化。
几种改变的氧化脂类具有已知或可疑的支气管保护或抗炎作用,这表明哮喘患者在暴露于地铁空气后可能会出现抗炎反应减弱。这些观察结果可能对城市地区的敏感亚群产生影响。