Combined exposure of diesel exhaust particles and respirable Soufrière Hills volcanic ash causes a (pro-)inflammatory response in an in vitro multicellular epithelial tissue barrier model.
Combined exposure of diesel exhaust particles and respirable Soufrière Hills volcanic ash causes a (pro-)inflammatory response in an in vitro multicellular epithelial tissue barrier model.
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在体外多细胞上皮组织屏障模型中，柴油排气颗粒和可呼吸的soufrière山丘陵的结合暴露会引起（促）炎症反应。
DOI：
10.1186/s12989-016-0178-9
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发表时间：
2016-12-12
影响因子：
10
通讯作者：
Clift MJ
中科院分区：
文献类型：
--
作者：
Tomašek I;Horwell CJ;Damby DE;Barošová H;Geers C;Petri-Fink A;Rothen-Rutishauser B;Clift MJ
人类接触火山灰颗粒可能产生的不利影响值得关注，特别是考虑到已经暴露于严重空气污染的城市地区的社区。因此，本研究的目的是首先了解与柴油颗粒同时暴露的可吸入性VA的生物影响。建立体外三维三细胞共培养人肺泡上皮组织屏障模型，在空气-液体界面（ALI）处暴露于单次或重复剂量的干呼吸性VA（沉积剂量分别为0.26±0.09或0.89±0.29 μg/cm2）。随后，在伪ali下，共同培养物暴露于单一或重复的VA和柴油废气颗粒（DEP; NIST SRM 2975; 0.02 mg/mL），这是一种典型的城市污染物。在这些精确的情景下，还分析了每种颗粒类型的生物影响。在颗粒暴露后评估细胞毒性（LDH释放），氧化应激（细胞内GSH的消耗）和（前）炎症（TNF-α， IL-8和IL-1β）反应。VA暴露对细胞形态的影响，以及它与多细胞模型的相互作用，分别通过共聚焦激光扫描显微镜（LSM）和扫描电子显微镜（SEM）进行可视化。在所有情况下，与单独暴露于VA相比，当以亚致死剂量施用于共培养时，可吸入VA和DEP的组合激发TNF-α和IL-8的释放增加，以及IL-1β的显著增加。值得注意的是，观察到的增强（促）炎症反应不是由氧化应激介导的。LSM支持细胞毒性的定量评估，在屏障模型中没有明显的细胞形态学变化。通过扫描电镜观察到VA与多细胞系统的所有三种细胞类型的直接相互作用。在一个先进的体外多细胞上皮气道屏障模型中，可呼吸性soufriires Hills VA与DEP联合暴露可引起（促）炎症作用。这一发现表明，应进一步调查火山和城市颗粒物质的联合暴露，以推断潜在的人类健康危害，特别是它如何影响人群中易感个体（即已有肺部疾病）的呼吸功能。本文的在线版本（doi:10.1186/s12989-016-0178-9）包含补充材料，可供授权用户使用。
There are justifiable health concerns regarding the potential adverse effects associated with human exposure to volcanic ash (VA) particles, especially when considering communities living in urban areas already exposed to heightened air pollution. The aim of this study was, therefore, to gain an imperative, first understanding of the biological impacts of respirable VA when exposed concomitantly with diesel particles. A sophisticated in vitro 3D triple cell co-culture model of the human alveolar epithelial tissue barrier was exposed to either a single or repeated dose of dry respirable VA (deposited dose of 0.26 ± 0.09 or 0.89 ± 0.29 μg/cm2, respectively) from Soufrière Hills volcano, Montserrat for a period of 24 h at the air-liquid interface (ALI). Subsequently, co-cultures were exposed to co-exposures of single or repeated VA and diesel exhaust particles (DEP; NIST SRM 2975; 0.02 mg/mL), a model urban pollutant, at the pseudo-ALI. The biological impact of each individual particle type was also analysed under these precise scenarios. The cytotoxic (LDH release), oxidative stress (depletion of intracellular GSH) and (pro-)inflammatory (TNF-α, IL-8 and IL-1β) responses were assessed after the particulate exposures. The impact of VA exposure upon cell morphology, as well as its interaction with the multicellular model, was visualised via confocal laser scanning microscopy (LSM) and scanning electron microscopy (SEM), respectively. The combination of respirable VA and DEP, in all scenarios, incited an heightened release of TNF-α and IL-8 as well as significant increases in IL-1β, when applied at sub-lethal doses to the co-culture compared to VA exposure alone. Notably, the augmented (pro-)inflammatory responses observed were not mediated by oxidative stress. LSM supported the quantitative assessment of cytotoxicity, with no changes in cell morphology within the barrier model evident. A direct interaction of the VA with all three cell types of the multicellular system was observed by SEM. Combined exposure of respirable Soufrière Hills VA with DEP causes a (pro-)inflammatory effect in an advanced in vitro multicellular model of the epithelial airway barrier. This finding suggests that the combined exposure to volcanic and urban particulate matter should be further investigated in order to deduce the potential human health hazard, especially how it may influence the respiratory function of susceptible individuals (i.e. with pre-existing lung diseases) in the population. The online version of this article (doi:10.1186/s12989-016-0178-9) contains supplementary material, which is available to authorized users.
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影响因子：
5.3
作者：
Horwell, C. J.;Fenoglio, I.;Fublni, B.
通讯作者：
Fublni, B.
影响因子：
120.7
作者：
Dominici, F;Peng, RD;Samet, JM
通讯作者：
Samet, JM
影响因子：
10
作者：
Endes C;Schmid O;Kinnear C;Mueller S;Camarero-Espinosa S;Vanhecke D;Foster EJ;Petri-Fink A;Rothen-Rutishauser B;Weder C;Clift MJ
通讯作者：
Clift MJ
影响因子：
3.5
作者：
Horwell, CJ;Sparks, RSJ;Williamson, BJ
通讯作者：
Williamson, BJ
影响因子：
3.5
作者：
Horwell, Claire J.;Le Blond, Jennifer S.;Cressey, Gordon
通讯作者：
Cressey, Gordon