Asian Sand Dust Enhances the Inflammatory Response and Mucin Gene Expression in the Middle Ear

Asia sand dust (ASD) is known to cause various human diseases including respiratory infection. The aim of this study was to examine the effect of ASD on inflammatory response in human middle ear epithelial cells (HMEECs) in vitro and in vivo. Cell viability was assessed using the cell counting kit-8...

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Published inClinical and experimental otorhinolaryngology Vol. 9; no. 3; pp. 198 - 205
Main Authors Chang, Jiwon, Go, Yoon Young, Park, Moo Kyun, Chae, Sung-Won, Lee, Seon-Heui, Song, Jae-Jun
Format Journal Article
LanguageEnglish
Published Korea (South) Korean Society of Otorhinolaryngology-Head and Neck Surgery 01.09.2016
대한이비인후과학회
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Summary:Asia sand dust (ASD) is known to cause various human diseases including respiratory infection. The aim of this study was to examine the effect of ASD on inflammatory response in human middle ear epithelial cells (HMEECs) in vitro and in vivo. Cell viability was assessed using the cell counting kit-8 assay. The mRNA levels of various genes including COX-2, TNF-a, MUC 5AC, MUC 5B, TP53, BAX, BCL-2, NOX4, and SOD1 were analyzed using semiquantitative realtime polymerase chain reaction. COX-2 protein levels were determined by western blot analysis. Sprague Dawley rats were used for in vivo investigations of inflammatory reactions in the middle ear epithelium as a result of ASD injection. We observed dose-dependent decrease in HMEEC viability. ASD exposure significantly increased COX-2, TNF-a, MUC5AC, and MUC5B mRNA expression. Also, ASD affected the mRNA levels of apoptosis- and oxidative stress-related genes. Western blot analysis revealed a dose-dependent increase in COX-2 production. Animal studies also demonstrated an ASD-induced inflammatory response in the middle ear epithelium. Environmental ASD exposure can result in the development of otitis media.
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The first two authors contributed equally to this study.
G704-SER000001014.2016.9.3.010
http://dx.doi.org/10.21053/ceo.2015.01060
ISSN:1976-8710
2005-0720
DOI:10.21053/ceo.2015.01060