Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States; Solomon H. Snyder Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Department of Health, Policy and Management, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States.
Environ Res. 2018 Feb;161:304-313. doi: 10.1016/j.envres.2017.10.041. Epub 2017 Nov 24.
Exposure to particulate matter (PM) is increasing worldwide as a result of increased human activity, the rapid industrialization of developing countries, and effects of climate change. Adverse effects of PM on human health are well documented, and because PM exposure occurs mostly through the airways, PM has especially deleterious impact on the lungs.
We investigated whether surrogate PM particles like carbon black (CB), diesel exhaust particle (DEP), coal fly ash (CFA) can recapitulate the allergic airway inflammatory response induced by urban particulate matter.
We compared the pro-inflammatory potential of urban PM collected from New York (NYC) and Baltimore (Balt) with CB, DEP and CFA surrogate PM particles. Eight to ten weeks old BALB/cJ mice were exposed through the airways to particulate material, and markers of airway inflammation were determined. Specifically, we assessed cellular influx, mucus production, lung function, cytokine levels as well as immune cell profiling of the lungs.
Herein, we demonstrate that exposure to equivalent mass of stand-alone surrogate PM particles like CB, DEP and CFA, fails to induce significant airway inflammatory response seen after similar exposure to urban PMs. Specifically, we observe that PM collected from New York (NYC) and Baltimore city (Balt) triggers a mixed Th2/Th17 response accompanied by eosinophilic and neutrophilic influx, mucus production and airway hyperresponsiveness (AHR). Although the immune profile of NYC and Baltimore PMs are similar, they demonstrate considerable differences in their potency. Baltimore PM induced more robust airway inflammation, AHR, and Th2 cytokine production, possibly due to the greater metal content in Baltimore PM.
Urban particulate matter with its unique physiochemical properties and heterogeneous composition elicits a mixed Th2/Th17 allergic airway response that is not seen after similar exposures to surrogate PM particles.
由于人类活动的增加、发展中国家的快速工业化以及气候变化的影响，世界各地的颗粒物（PM）暴露量正在增加。PM 对人类健康的不良影响已有充分记录，并且由于 PM 暴露主要通过呼吸道发生，因此 PM 对肺部的危害尤其严重。
我们研究了像炭黑（CB）、柴油尾气颗粒（DEP）、煤飞灰（CFA）这样的替代 PM 颗粒是否可以重现由城市颗粒物引起的过敏性气道炎症反应。
我们比较了从纽约（NYC）和巴尔的摩（Balt）收集的城市 PM 与 CB、DEP 和 CFA 替代 PM 颗粒的促炎潜力。将 8 到 10 周龄的 BALB/cJ 小鼠通过呼吸道暴露于颗粒物，并测定气道炎症标志物。具体而言，我们评估了细胞浸润、黏液产生、肺功能、细胞因子水平以及肺部免疫细胞谱。
在这里，我们证明暴露于单独的替代 PM 颗粒（如 CB、DEP 和 CFA）等效质量，无法引起类似于暴露于城市 PM 后观察到的明显气道炎症反应。具体而言，我们观察到从纽约（NYC）和巴尔的摩市（Balt）收集的 PM 引发了混合的 Th2/Th17 反应，伴随着嗜酸性粒细胞和中性粒细胞浸润、黏液产生和气道高反应性（AHR）。尽管 NYC 和 Baltimore PM 的免疫谱相似，但它们的效力却存在很大差异。Baltimore PM 引起了更强烈的气道炎症、AHR 和 Th2 细胞因子产生，这可能是由于 Baltimore PM 中含有更多的金属。
具有独特理化性质和异质组成的城市颗粒物会引发混合的 Th2/Th17 过敏性气道反应，而类似暴露于替代 PM 颗粒则不会引起这种反应。
