Ambient particulate matter (PM) is associated with adverse health consequences. However, the influence of PM on the innate immune system is poorly understood. The aim of the present study was to examine the effect of diesel particulate matter 2.5 μm (PM_2.5, SRM1650b) on dendritic cells. PM_2.5 significantly reduced cytokine levels of interleukin (IL)-12 p40, IL-6 and TNF-α levels in CpG-DNA (TLR9 ligand)-stimulated dendritic cells. To determine the mechanisms underlying this observed inhibition induced by PM_2.5, western blot analysis was conducted. PM_2.5 was found to downregulate ERK1/2, JNK1/2, p38 MAPKs, and NF-κB pathways. PM_2.5 exposure decreased TLR9-dependent NF-κB and activator protein (AP-1) reporter luciferase activities. Our findings demonstrate that PM_2.5 reduced the production of cytokines which may be associated with inhibition of MAPK and NF-κB signaling pathway. Further, data suggest the immunosuppressive effect of PM_2.5 on the innate immune cells may lead to serious damage to the host immune system.

环境颗粒物（PM）与不良健康后果相关。但是，人们对PM对先天免疫系统的影响知之甚少。本研究的目的是研究2.5μm柴油颗粒物（PM _2.5，SRM1650b）对树突状细胞的影响。PM _2.5显着降低了CpG-DNA（TLR9配体）刺激的树突状细胞中白介素（IL）-12 p40，IL-6和TNF-α的细胞因子水平。为了确定这种观察到的由PM _2.5诱导的抑制的机制，进行了蛋白质印迹分析。发现PM _2.5下调ERK1 / 2，JNK1 / 2，p38 MAPK和NF-κB通路。下午_2.5暴露会降低TLR9依赖性NF-κB和激活蛋白（AP-1）报告荧光素酶的活性。我们的发现表明，PM _2.5减少了可能与抑制MAPK和NF-κB信号通路有关的细胞因子的产生。此外，数据表明PM _2.5对先天免疫细胞的免疫抑制作用可能导致对宿主免疫系统的严重破坏。