Particulate matter (PM) air pollution has been associated with an increase in the incidence of chronic allergic diseases; however, the mechanisms underlying the effect of exposure to natural ambient air pollution in chronic allergic diseases have not been fully elucidated. In the present study, we aimed to investigate the cellular responses induced by exposure to natural ambient air pollution, employing a mouse model of chronic allergy. The results indicated that exposure to ambient air pollution significantly increased the number of eosinophils in the nasal mucosa. The modulation of gene expression profile identified a set of regulated genes, and the Triggering Receptor Expressed on Myeloid cells1(TREM1) signaling canonical pathway was increased after exposure to ambient air pollution. In vitro, PM2.5 increased Nucleotide-binding oligomerization domain-containing protein 1 (Nod1) and nuclear factor (NF)-κB signaling pathway activation in A549 and HEK293 cell cultures. These results suggest a novel mechanism by which, PM2.5 in ambient air pollution may stimulate the innate immune system through the PM2.5-Nod1-NF-κB axis in chronic allergic disease.

中文翻译：

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暴露于自然环境中富含PM2.5的环境空气污染的慢性过敏小鼠模型中基因表达的变化。

颗粒物（PM）空气污染与慢性过敏性疾病的发生率增加有关；然而，尚未完全阐明暴露于慢性过敏性疾病中的自然环境空气污染的潜在机制。在本研究中，我们旨在研究慢性过敏的小鼠模型，研究暴露于自然环境空气污染引起的细胞反应。结果表明，暴露于环境空气污染显着增加了鼻黏膜中嗜酸性粒细胞的数量。基因表达谱的调控识别出一组受调控的基因，暴露于空气污染后，髓样细胞1（TREM1）信号传导途径上的触发受体表达增加。体外，PM2。5在A549和HEK293细胞培养物中增加了含有核苷酸结合的寡聚域的蛋白1（Nod1）和核因子（NF）-κB信号通路的激活。这些结果提示了一种新的机制，在这种机制中，环境空气中的PM2.5可以通过慢性过敏性疾病中的PM2.5-Nod1-NF-κB轴刺激先天免疫系统。