Effect of acrolein, a hazardous air pollutant in smoke, on human middle ear epithelial cells

Jae-Jun Song, Jong Dae Lee, Byung Don Lee, Sungwon Chae, Moo Kyun Park

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Objective: Acrolein is a hazardous air pollutant. Tobacco smoke and indoor air pollution are the main causes of human exposure. Acrolein has been shown to cause cytotoxicity in the airways and induce inflammation and mucin production in pulmonary cells. We investigated whether acrolein caused cytotoxicity, induced inflammation or increased expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Methods: Cytotoxicity following acrolein treatment was investigated using the MTT assay, flow cytometry, and Hoechst 33342 staining of HMEECs. We measured expression of inflammatory cytokines tumor necrosis factor (TNF)-α and cyclo-oxygenase (COX)-2 and the mucin gene MUC5AC using semi-quantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. Results: Exposure to >50. μg/mL acrolein caused a decrease in cell viability. Acrolein induced apoptosis and necrosis at 50. μg/mL. Acrolein at 5-50. μg/mL increased expression of TNF-α and COX-2, as shown by RT-PCR and Western blotting. Acrolein exposure at 5-50. μg/mL for 2-24. h increased MUC5AC expression, as determined by RT-PCR. Conclusion: Acrolein decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that acrolein, a hazardous air pollutant in tobacco smoke and ambient air, is a risk factor for otitis media.

Original languageEnglish
Pages (from-to)1659-1664
Number of pages6
JournalInternational Journal of Pediatric Otorhinolaryngology
Volume77
Issue number10
DOIs
Publication statusPublished - 2013 Oct 1

Fingerprint

Acrolein
Air Pollutants
Middle Ear
Smoke
Epithelial Cells
Mucins
Reverse Transcriptase Polymerase Chain Reaction
Prostaglandin-Endoperoxide Synthases
Cell Line
Cell Survival
Mucin-2
Tumor Necrosis Factor-alpha
Western Blotting
Indoor Air Pollution
Inflammation
Tobacco Smoke Pollution
Otitis Media
Tobacco
Real-Time Polymerase Chain Reaction
Flow Cytometry

Keywords

  • Acrolein
  • Human middle ear epithelial cells
  • Middle ear
  • Otitis media

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Pediatrics, Perinatology, and Child Health

Cite this

Effect of acrolein, a hazardous air pollutant in smoke, on human middle ear epithelial cells. / Song, Jae-Jun; Lee, Jong Dae; Lee, Byung Don; Chae, Sungwon; Park, Moo Kyun.

In: International Journal of Pediatric Otorhinolaryngology, Vol. 77, No. 10, 01.10.2013, p. 1659-1664.

Research output: Contribution to journalArticle

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N2 - Objective: Acrolein is a hazardous air pollutant. Tobacco smoke and indoor air pollution are the main causes of human exposure. Acrolein has been shown to cause cytotoxicity in the airways and induce inflammation and mucin production in pulmonary cells. We investigated whether acrolein caused cytotoxicity, induced inflammation or increased expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Methods: Cytotoxicity following acrolein treatment was investigated using the MTT assay, flow cytometry, and Hoechst 33342 staining of HMEECs. We measured expression of inflammatory cytokines tumor necrosis factor (TNF)-α and cyclo-oxygenase (COX)-2 and the mucin gene MUC5AC using semi-quantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. Results: Exposure to >50. μg/mL acrolein caused a decrease in cell viability. Acrolein induced apoptosis and necrosis at 50. μg/mL. Acrolein at 5-50. μg/mL increased expression of TNF-α and COX-2, as shown by RT-PCR and Western blotting. Acrolein exposure at 5-50. μg/mL for 2-24. h increased MUC5AC expression, as determined by RT-PCR. Conclusion: Acrolein decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that acrolein, a hazardous air pollutant in tobacco smoke and ambient air, is a risk factor for otitis media.

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