Department of Life Science, Institute of Environmental Medicine for Green Chemistry, Dongguk University Biomedi Campus, 32 Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do, 10326, Republic of Korea.
Department of Otorhinolaryngology, Head and Neck Surgery, Seoul National University Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Sci Rep. 2020 Oct 12;10(1):16972. doi: 10.1038/s41598-020-74109-6.
Airborne pollutants have detrimental effect on the human body and the environment. Diesel exhaust particles (DEPs) are known to be major component of particulate matter (PM) and cause respiratory diseases and neurotoxicity. However, the effects of air pollutants on the sensory nervous system, especially on the olfactory sense, have not been well studied. Herein, we aimed to explore DEP-induced changes in the olfactory perception process. Olfactory sensitivity test was performed after DEP inhalation in mice. Microarray was conducted to determine the differentially expressed genes, which were then utilized to build a network focused on neurotoxicity. Exposure to DEPs significantly reduced sniffing in mice, indicating a disturbance in the olfactory perception process. Through network analysis, we proposed five genes (Cfap69, Cyp26b1, Il1b, Il6, and Synpr) as biomarker candidates for DEP-mediated olfactory dysfunction. Changes in their expression might provoke malfunction of sensory transduction by inhibiting olfactory receptors, neurite outgrowth, and axonal guidance as well as lead to failure of recovery from neuroinflammatory damage through inhibition of nerve regeneration. Thus, we suggest the potential mechanism underlying DEPs-mediated olfactory disorders using genomic approach. Our study will be helpful to future researchers to assess an individual's olfactory vulnerability following exposure to inhalational environmental hazards.
空气中的污染物对人体和环境都有不良影响。柴油废气颗粒（DEP）是颗粒物（PM）的主要成分之一，会导致呼吸道疾病和神经毒性。然而，空气污染物对感觉神经系统的影响，特别是嗅觉，尚未得到充分研究。在此，我们旨在探讨 DEP 引起的嗅觉感知过程变化。在小鼠吸入 DEP 后进行嗅觉敏感性测试。进行微阵列分析以确定差异表达基因，然后利用这些基因构建一个专注于神经毒性的网络。DEP 的暴露显著降低了小鼠的嗅探，表明嗅觉感知过程受到干扰。通过网络分析，我们提出了五个基因（Cfap69、Cyp26b1、Il1b、Il6 和 Synpr）作为 DEP 介导的嗅觉功能障碍的生物标志物候选基因。它们的表达变化可能通过抑制嗅觉受体、神经突生长和轴突导向，以及通过抑制神经再生导致神经炎症损伤的恢复失败，从而引发感觉转导的功能障碍。因此，我们使用基因组方法提出了 DEP 介导的嗅觉障碍的潜在机制。我们的研究将有助于未来的研究人员评估个体在暴露于吸入性环境危害后嗅觉的脆弱性。
