Studies for the adverse effects of environmental nanoparticles on sensitive pulmonary diseases

事实上，我们吸入环境空气中的悬浮DEP和/或纳米颗粒然而，从未对吸入/气管内暴露于柴油发动机衍生纳米颗粒的影响进行评估，这是一种更现实的暴露，对肺部炎症模型的影响从未进行过。此外，据我们所知，还没有研究检查吸入纳米颗粒对易感受试者的剂量依赖性影响。本研究调查了肺暴露于柴油发动机衍生纳米颗粒对肺气肿肺损伤和过敏性呼吸道炎症的影响，并对其潜在机制进行了探讨。在第一次实验中，14 nm的CBNP显著地诱导了非诱导者的急性肺炎症，并在早期加重了PPE诱导的中性粒细胞炎症，同时伴随着肺组织促炎细胞因子表达的增强。在接下来的实验中，高浓度的NR-DE显著加重了OVA诱导的嗜酸性气道炎症。另一方面，DE气体不影响PPE诱导的肺气肿的肺部炎症反应。在体外实验中，NR-DEP显著增强BEAS-2B细胞上粘蛋白-1的表达以及小鼠脾细胞和树突状细胞表面CD86的表达。

In reality, we inhale suspended DEP and/or nanoparticles in ambient air Nevertheless, assessment of the impact of inhalation/intratracheal exposure to diesel engine-derived nanoparticles, a more realistic exposure, on the lung inflammation model has never been conducted. Furthermore, as far as we know, no study has examined the dose-dependent effects of inhaled nanoparticles on predisposed subjects. The present study investigated the impact of pulmonary exposure to diesel-engine-derived nanoparticles on emphysematous lung injury and allergic airway inflammation and dissolved its underlying mechanisms. In the first experiments, CBNP of 14 nm significantly induced acute lung inflammation in non-elicited subjects, and aggravated PPE-elicited airway neutrophilic inflammation at an early stage, which was concomitant with the enhanced lung expression of proinflammatory cytokines. In the next experiments, high concentration of NR-DE significantly deteriorated OVA-induced eosinophilic airway inflammation. On the other hand, DE gas did not influence PPE-induced pulmonary inflammation with emphysema. In in vitro experiments, NR-DEP significantly enhanced mucin-1 expression on BEAS-2B cells and surface expression of CD86 on mouse-derived splenocytes and dendritic cells.