Effects of cigarette smoking on mucin production in human middle ear epithelial cells

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15 Citations (Scopus)

Abstract

Objective: Otitis media (OM) is the most common disease in preschool age children related to passive cigarette smoking as risk factor. In this study, we investigate whether the cigarette smoking can induce the inflammation in human middle ear epithelial cell, and cigarette smoke-induced inflammation can increase the expression of MUC5AC gene and protein that was known to play an important role in OM with effusion. Methods: After treatment of cigarette smoke solution (CSS) on immortalized human middle ear epithelial cells (HMEECs) with or without pretreatment by epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (AG1478), we observed expression of tumor necrosis factor-alpha (TNF-α), EGFR, MUC5AC mRNA by quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and EGFR, MUC5AC protein by western blotting. Results: Treatment of CSS increased expression of TNF-α mRNA dose dependently. Treatment of CSS upregulated the EGFR and MUC5AC mRNA in a time-dependent manner. CSS-induced upregulation of EGFR and MUC5AC mRNA was suppressed by the pretreatment of AG1478. EGFR and MUC5AC proteins were upregulated by the treatment of CSS and suppressed by the pretreatment of AG1478. Conclusions: Treatment of CSS on HMEECs increased the expression of MUC5AC mRNAs and proteins which play a major role in OM with effusion.

Original languageEnglish
Pages (from-to)1447-1451
Number of pages5
JournalInternational Journal of Pediatric Otorhinolaryngology
Volume73
Issue number10
DOIs
Publication statusPublished - 2009 Oct 1

Fingerprint

Mucins
Middle Ear
Smoke
Tobacco Products
Epidermal Growth Factor Receptor
Smoking
Epithelial Cells
Messenger RNA
Otitis Media with Effusion
Proteins
Tumor Necrosis Factor-alpha
Inflammation
Therapeutics
Tobacco Smoke Pollution
Otitis Media
Preschool Children
Reverse Transcriptase Polymerase Chain Reaction
Protein-Tyrosine Kinases
Real-Time Polymerase Chain Reaction
Up-Regulation

Keywords

  • Epidermal growth factor receptor
  • Human middle ear epithelial cells
  • MUC5AC
  • Otitis media
  • Smoking

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Pediatrics, Perinatology, and Child Health

Cite this

@article{801a467345a046009cfef6c62f26d445,
title = "Effects of cigarette smoking on mucin production in human middle ear epithelial cells",
abstract = "Objective: Otitis media (OM) is the most common disease in preschool age children related to passive cigarette smoking as risk factor. In this study, we investigate whether the cigarette smoking can induce the inflammation in human middle ear epithelial cell, and cigarette smoke-induced inflammation can increase the expression of MUC5AC gene and protein that was known to play an important role in OM with effusion. Methods: After treatment of cigarette smoke solution (CSS) on immortalized human middle ear epithelial cells (HMEECs) with or without pretreatment by epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (AG1478), we observed expression of tumor necrosis factor-alpha (TNF-α), EGFR, MUC5AC mRNA by quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and EGFR, MUC5AC protein by western blotting. Results: Treatment of CSS increased expression of TNF-α mRNA dose dependently. Treatment of CSS upregulated the EGFR and MUC5AC mRNA in a time-dependent manner. CSS-induced upregulation of EGFR and MUC5AC mRNA was suppressed by the pretreatment of AG1478. EGFR and MUC5AC proteins were upregulated by the treatment of CSS and suppressed by the pretreatment of AG1478. Conclusions: Treatment of CSS on HMEECs increased the expression of MUC5AC mRNAs and proteins which play a major role in OM with effusion.",
keywords = "Epidermal growth factor receptor, Human middle ear epithelial cells, MUC5AC, Otitis media, Smoking",
author = "Jae-Gu Cho and Jeong-Soo Woo and Lee, {Heung Man} and Jung, {Hak Hyun} and Hwang, {Soon Jae} and Sungwon Chae",
year = "2009",
month = "10",
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language = "English",
volume = "73",
pages = "1447--1451",
journal = "International Journal of Pediatric Otorhinolaryngology",
issn = "0165-5876",
publisher = "Elsevier Ireland Ltd",
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T1 - Effects of cigarette smoking on mucin production in human middle ear epithelial cells

AU - Cho, Jae-Gu

AU - Woo, Jeong-Soo

AU - Lee, Heung Man

AU - Jung, Hak Hyun

AU - Hwang, Soon Jae

AU - Chae, Sungwon

PY - 2009/10/1

Y1 - 2009/10/1

N2 - Objective: Otitis media (OM) is the most common disease in preschool age children related to passive cigarette smoking as risk factor. In this study, we investigate whether the cigarette smoking can induce the inflammation in human middle ear epithelial cell, and cigarette smoke-induced inflammation can increase the expression of MUC5AC gene and protein that was known to play an important role in OM with effusion. Methods: After treatment of cigarette smoke solution (CSS) on immortalized human middle ear epithelial cells (HMEECs) with or without pretreatment by epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (AG1478), we observed expression of tumor necrosis factor-alpha (TNF-α), EGFR, MUC5AC mRNA by quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and EGFR, MUC5AC protein by western blotting. Results: Treatment of CSS increased expression of TNF-α mRNA dose dependently. Treatment of CSS upregulated the EGFR and MUC5AC mRNA in a time-dependent manner. CSS-induced upregulation of EGFR and MUC5AC mRNA was suppressed by the pretreatment of AG1478. EGFR and MUC5AC proteins were upregulated by the treatment of CSS and suppressed by the pretreatment of AG1478. Conclusions: Treatment of CSS on HMEECs increased the expression of MUC5AC mRNAs and proteins which play a major role in OM with effusion.

AB - Objective: Otitis media (OM) is the most common disease in preschool age children related to passive cigarette smoking as risk factor. In this study, we investigate whether the cigarette smoking can induce the inflammation in human middle ear epithelial cell, and cigarette smoke-induced inflammation can increase the expression of MUC5AC gene and protein that was known to play an important role in OM with effusion. Methods: After treatment of cigarette smoke solution (CSS) on immortalized human middle ear epithelial cells (HMEECs) with or without pretreatment by epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (AG1478), we observed expression of tumor necrosis factor-alpha (TNF-α), EGFR, MUC5AC mRNA by quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and EGFR, MUC5AC protein by western blotting. Results: Treatment of CSS increased expression of TNF-α mRNA dose dependently. Treatment of CSS upregulated the EGFR and MUC5AC mRNA in a time-dependent manner. CSS-induced upregulation of EGFR and MUC5AC mRNA was suppressed by the pretreatment of AG1478. EGFR and MUC5AC proteins were upregulated by the treatment of CSS and suppressed by the pretreatment of AG1478. Conclusions: Treatment of CSS on HMEECs increased the expression of MUC5AC mRNAs and proteins which play a major role in OM with effusion.

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