Asian Sand Dust Enhances the Inflammatory Response and Mucin Gene Expression in the Middle Ear
1
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
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-α, MUC5AC, MUC5B, TP53, BAX, BCL-2, NOX4, and SOD1 were analyzed using semiquantitative real-time 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-α, 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.
Abstract
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-α, MUC5AC, MUC5B, TP53, BAX, BCL-2, NOX4, and SOD1 were analyzed using semiquantitative real-time 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-α, 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.
참고문헌 (21)
- yadav mukesh kumar, "In Vitro Streptococcus pneumoniae Biofilm Formation and In Vivo Middle Ear Mucosal Biofilm in a Rat Model of Acute Otitis Induced by S. pneumoniae", Clinical and Experimental Otorhinolaryngology, 5(3), pp.139~144 (2012), 대한이비인후과학회[DOI]
- Ribeiro H., "Air pollution and children’s health in São Paulo(1986-1998)", Soc Sci Med, 57(11), pp.2013~2022 (2003)
- Dostal M., "Childhood morbidity and air pollution in the Teplice program", Cas Lek Cesk, 140(21), pp.658~661 (2001)
- Rovers MM., "Risk factors for otitis media : an international perspective", Int J Pediatr Otorhinolaryngol, 70(7), pp.1251~1256 (2006)
- Heinrich J., "Environmental surveys in the areas of Bitterfeld, Hettstedt and a comparative area in 1992-2000", Gesundheitswesen, 64(12), pp.675~682 (2002)
- 강일규, "Asian Sand Dust Enhances Allergen-Induced Th2 Allergic Inflammatory Changes and Mucin Production in BALB", c Mouse Lungs, 2012, pp.4(4), 206~213[DOI]
- Chen YS., "Effects of Asian dust storm events on daily hospital admissions for cardiovascular disease in Taipei, Taiwan", J Toxicol Environ Health A, 68(17-18), pp.1457~1464 (2005)
- Honda A., "Effects of Asian sand dust particles on the respiratory and immune system", J Appl Toxicol, Mar, 34(3), pp.250~257 (2014)
- Chun YM., "Immortalization of normal adult human middle ear epithelial cells using a retrovirus containing the E6", E7 genes of human papillomavirus type 16, 2002, pp.111(6), 507~517
- Hoek G., "Long-term air pollution exposure and cardio-respiratory mortality : a review", Environ Health, 12(1), pp.43~ (2013)
- Huang YC., "Comparison of gene expression profiles induced by coarse, fine, and ultrafine particulate matter", J Toxicol Environ Health A, 74(5), pp.296~312 (2011)
- Hiyoshi K., "Asian sand dust enhances ovalbumin-induced eosinophil recruitment in the alveoli and airway of mice", Environ Res, 99(3), pp.361~368 (2005)
- Caceres Udina MJ., "Incidence, air pollution and risk factors of acute otitis media in the first year of life : a prospective study", An Pediatr (Barc), 60(2), pp.133~138 (2004)
- Preciado D., "Cigarette smoke activates NFκB-mediated Tnf-α release from mouse middle ear cells", Laryngoscope, 120(12), pp.2508~2515 (2010)
- Kakiuchi M., "Cyclooxygenase 2 expression in otitis media with effusion", Am J Otolaryngol, 27(2), pp.81~85 (2006)
- Medeiros R., "The role of TNF-alpha signaling pathway on COX-2 upregulation and cognitive decline induced by beta-amyloid peptide", Behav Brain Res, 209(1), pp.165~173 (2010)
- Kim ST., "Effects of Asian sand dust on mucin gene expression and activation of nasal polyp epithelial cells", Am J Rhinol Allergy, 25(5), pp.303~306 (2011)
- Fahy JV., "Airway mucus function and dysfunction", N Engl J Med, 363(23), pp.2233~2247 (2010)
- Roy MG., "Muc5b is required for airway defence", Nature, 505(7483), pp.412~416 (2014)
- Kawano H., "Identification of MUC5B mucin gene in human middle ear with chronic otitis media", Laryngoscope, 110(4), pp.668~673 (2000)
- Cho JG., "Effects of cigarette smoking on mucin production in human middle ear epithelial cells", Int J Pediatr Otorhinolaryngol, 73(10), pp.1447~1451 (2009)