Effect of diesel exhaust particles 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

28 Citations (Scopus)

Abstract

Objective: In the present study, we investigate whether diesel exhaust particles (DEPs) cause cytotoxicity and induce inflammation or increase the expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Several publications have shown an association between traffic-related air pollutants and otitis media. Additionally, DEP have been shown to cause inflammation and an allergic response in the airways. Methods: Cell viability following DEP treatment was investigated in HMEECs using the MTT assay. We measured the expression of the inflammatory cytokines TNF-α and COX-2 and the mucin genes MUC5AC and MUC5B using semiquantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. Results: Cell viability tests showed that exposure to more than 80 μg/mL of DEP caused a decrease in cell viability. DEP exposure also increased the expression of MUC5AC, but did not induce the expression of MUC5B in HMEECs. Conclusion: DEP decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that environmental diesel exposure is a risk factor for otitis media.

Original languageEnglish
Pages (from-to)334-338
Number of pages5
JournalInternational Journal of Pediatric Otorhinolaryngology
Volume76
Issue number3
DOIs
Publication statusPublished - 2012 Mar 1

Fingerprint

Vehicle Emissions
Middle Ear
Epithelial Cells
Cell Survival
Cell Line
Otitis Media
Mucins
Mucin-2
Inflammation
Air Pollutants
Environmental Exposure
Reverse Transcriptase Polymerase Chain Reaction
Publications
Real-Time Polymerase Chain Reaction
Western Blotting
Cytokines
Gene Expression
Genes

Keywords

  • Diesel
  • Human middle ear epithelial cells
  • Otitis media

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Otorhinolaryngology

Cite this

Effect of diesel exhaust particles 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. 76, No. 3, 01.03.2012, p. 334-338.

Research output: Contribution to journalArticle

@article{f6540d562d9e4db7899498dc6678d5bb,
title = "Effect of diesel exhaust particles on human middle ear epithelial cells",
abstract = "Objective: In the present study, we investigate whether diesel exhaust particles (DEPs) cause cytotoxicity and induce inflammation or increase the expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Several publications have shown an association between traffic-related air pollutants and otitis media. Additionally, DEP have been shown to cause inflammation and an allergic response in the airways. Methods: Cell viability following DEP treatment was investigated in HMEECs using the MTT assay. We measured the expression of the inflammatory cytokines TNF-α and COX-2 and the mucin genes MUC5AC and MUC5B using semiquantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. Results: Cell viability tests showed that exposure to more than 80 μg/mL of DEP caused a decrease in cell viability. DEP exposure also increased the expression of MUC5AC, but did not induce the expression of MUC5B in HMEECs. Conclusion: DEP decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that environmental diesel exposure is a risk factor for otitis media.",
keywords = "Diesel, Human middle ear epithelial cells, Otitis media",
author = "Jae-Jun Song and Lee, {Jong Dae} and Lee, {Byung Don} and Sungwon Chae and Park, {Moo Kyun}",
year = "2012",
month = "3",
day = "1",
doi = "10.1016/j.ijporl.2011.12.003",
language = "English",
volume = "76",
pages = "334--338",
journal = "International Journal of Pediatric Otorhinolaryngology",
issn = "0165-5876",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

TY - JOUR

T1 - Effect of diesel exhaust particles on human middle ear epithelial cells

AU - Song, Jae-Jun

AU - Lee, Jong Dae

AU - Lee, Byung Don

AU - Chae, Sungwon

AU - Park, Moo Kyun

PY - 2012/3/1

Y1 - 2012/3/1

N2 - Objective: In the present study, we investigate whether diesel exhaust particles (DEPs) cause cytotoxicity and induce inflammation or increase the expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Several publications have shown an association between traffic-related air pollutants and otitis media. Additionally, DEP have been shown to cause inflammation and an allergic response in the airways. Methods: Cell viability following DEP treatment was investigated in HMEECs using the MTT assay. We measured the expression of the inflammatory cytokines TNF-α and COX-2 and the mucin genes MUC5AC and MUC5B using semiquantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. Results: Cell viability tests showed that exposure to more than 80 μg/mL of DEP caused a decrease in cell viability. DEP exposure also increased the expression of MUC5AC, but did not induce the expression of MUC5B in HMEECs. Conclusion: DEP decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that environmental diesel exposure is a risk factor for otitis media.

AB - Objective: In the present study, we investigate whether diesel exhaust particles (DEPs) cause cytotoxicity and induce inflammation or increase the expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Several publications have shown an association between traffic-related air pollutants and otitis media. Additionally, DEP have been shown to cause inflammation and an allergic response in the airways. Methods: Cell viability following DEP treatment was investigated in HMEECs using the MTT assay. We measured the expression of the inflammatory cytokines TNF-α and COX-2 and the mucin genes MUC5AC and MUC5B using semiquantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. Results: Cell viability tests showed that exposure to more than 80 μg/mL of DEP caused a decrease in cell viability. DEP exposure also increased the expression of MUC5AC, but did not induce the expression of MUC5B in HMEECs. Conclusion: DEP decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that environmental diesel exposure is a risk factor for otitis media.

KW - Diesel

KW - Human middle ear epithelial cells

KW - Otitis media

UR - http://www.scopus.com/inward/record.url?scp=84856776277&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84856776277&partnerID=8YFLogxK

U2 - 10.1016/j.ijporl.2011.12.003

DO - 10.1016/j.ijporl.2011.12.003

M3 - Article

C2 - 22209256

AN - SCOPUS:84856776277

VL - 76

SP - 334

EP - 338

JO - International Journal of Pediatric Otorhinolaryngology

JF - International Journal of Pediatric Otorhinolaryngology

SN - 0165-5876

IS - 3

ER -