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Gene Expression Analysis to Investigate Biological Networks Underlying Nasal Inflammatory Dysfunctions Induced by Diesel Exhaust Particles Using an In Vivo System

Authors
Kim, Hyun SooKim, Byeong-GonPark, SohyeonKim, NahyunJang, An-SooSeo, Young RokPark, Moo Kyun
Issue Date
Mar-2020
Publisher
Annals Publishing Co.
Keywords
air pollution; diesel exhaust particles; inflammation; microarray; nasal damages
Citation
Annals of Otology, Rhinology and Laryngology, v.129, no.3, pp 245 - 255
Pages
11
Journal Title
Annals of Otology, Rhinology and Laryngology
Volume
129
Number
3
Start Page
245
End Page
255
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/3075
DOI
10.1177/0003489419883289
ISSN
0003-4894
1943-572X
Abstract
Objectives: 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 in vitro, 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 vivo. Methods: 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. Results: 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. Conclusions: Although further mechanistic studies are required for verifying the utility of the potential biomarkers suggested by the present study, our in vivo results may provide meaningful suggestions for understanding the complex cellular signaling pathways involved in DEP-induced nasal damages.
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