Kim Hyun Soo, Kim Byeong-Gon, Park Sohyeon, Kim Nahyun, Jang An-Soo, Seo Young Rok, Park Moo Kyun
Institute of Environmental Medicine, Department of Life Science, Dongguk University Biomedi Campus, Goyang-si, Gyeonggi-do, Republic of Korea.
Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University College of Medicine, Seoul, Republic of Korea.
Ann Otol Rhinol Laryngol. 2020 Mar;129(3):245-255. doi: 10.1177/0003489419883289. Epub 2019 Oct 24.
Diesel exhaust particles (DEP)s are notorious ambient pollutants composed of a complex mixture of a carbon core and diverse chemical irritants. Several studies have demonstrated significant relationships between DEP exposure and serious nasal inflammatory response , but available information regarding underlying networks in terms of gene expression changes has not sufficiently explained potential mechanisms of DEP-induced nasal damage, especially .
In the present study, we identified DEP-induced gene expression profiles under short-term and long-term exposure, and identified signaling pathways based on microarray data for understanding effects of DEP exposure in the mouse nasal cavity.
Alteration in gene expression due to DEP exposure provokes an imbalance of the immune system via dysregulated inflammatory markers, predicted to disrupt protective responses against harmful exogenous substances in the body. Several candidate markers were identified after validation using qRT-PCR, including S100A9, CAMP, IL20, and S100A8.
Although further mechanistic studies are required for verifying the utility of the potential biomarkers suggested by the present study, our results may provide meaningful suggestions for understanding the complex cellular signaling pathways involved in DEP-induced nasal damages.
柴油尾气颗粒（DEP）是一种臭名昭著的环境污染物，由碳核和多种化学刺激物组成的复杂混合物构成。多项研究表明DEP暴露与严重的鼻腔炎症反应之间存在显著关联，但关于基因表达变化潜在网络的现有信息尚未充分解释DEP诱导鼻腔损伤的潜在机制。
在本研究中，我们确定了短期和长期暴露下DEP诱导的基因表达谱，并基于微阵列数据确定信号通路，以了解DEP暴露对小鼠鼻腔的影响。
DEP暴露导致的基因表达改变通过炎症标志物失调引发免疫系统失衡，预计会破坏机体对有害外源物质的保护反应。使用qRT-PCR验证后确定了几个候选标志物，包括S100A9、CAMP、IL20和S100A8。
尽管需要进一步的机制研究来验证本研究提出的潜在生物标志物的效用，但我们的结果可能为理解DEP诱导鼻腔鼻腔损伤中涉及的复杂细胞信号通路提供有意义的建议。
