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Published on: June 14, 2016
Asian Sand Dust Enhances the Inflammatory Response and Mucin Gene Expression in the Middle Ear
Jiwon Chang1, Yoon Young Go2, Moo Kyun Park3
1Department of Otolaryngology-Head and Neck Surgery, Hallym University College of Medicine, Seoul, Korea.
Objectives:
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.
Methods:
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.
Results:
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.
Conclusion:
Environmental ASD exposure can result in the development of otitis media.
Insights
Asia sand dust (ASD) exposure causes inflammation and cell damage in middle ear epithelial cells. This study shows ASD can lead to otitis media, impacting respiratory health.
Area of Science:
- Environmental Science
- Cell Biology
- Otolaryngology
Background:
- Asia sand dust (ASD) is linked to respiratory illnesses.
- The impact of ASD on middle ear inflammation is not well understood.
Purpose of the Study:
- To investigate the effects of ASD on human middle ear epithelial cells (HMEECs) in vitro.
- To examine the in vivo inflammatory response in the middle ear epithelium due to ASD exposure.
Main Methods:
- Assessed HMEEC viability using the cell counting kit-8 assay.
- Analyzed gene expression (COX-2, TNF-a, MUC5AC, MUC5B, apoptosis, oxidative stress markers) via real-time PCR.
- Determined COX-2 protein levels using Western blot.
- Investigated ASD-induced inflammation in Sprague Dawley rats.
Main Results:
- ASD exposure decreased HMEEC viability in a dose-dependent manner.
- Significantly increased mRNA expression of COX-2, TNF-a, MUC5AC, and MUC5B.
- Altered expression of apoptosis and oxidative stress-related genes.
- Elevated COX-2 protein levels and demonstrated ASD-induced middle ear inflammation in vivo.
Conclusions:
- ASD exposure induces inflammatory responses in the middle ear.
- Environmental ASD exposure may contribute to the development of otitis media.
