The cigarette smoke component acrolein inhibits expression of the innate immune components IL-8 and human beta-defensin 2 by sinonasal epithelial cells

Research output: Contribution to journalArticle

Abstract

Background: Tobacco use is associated with poorer outcomes of medical and surgical therapy for chronic rhinosinusitis (CRS), although the underlying mechanism is unknown. Acrolein (AC) is a major component of cigarette smoke that has been shown to suppress innate immune gene expression by human bronchial epithelial cells and murine macrophages. In this study, we explore whether exposure of human sinonasal epithelial cells (HSNECs) to AC similarly reduces their innate immune gene expression. Methods: Primary HSNECs from CRS patients were grown in culture, either differentiated or submerged. HSNECs were treated for 30 minutes with 0-50 μM of AC and were subsequently analyzed by real-time polymerase chain reaction and ELISA to determine IL-8 and human beta-defensin (HBD) 2 expression. Total glutathione was measured to see the oxidative stress within the treatment range. Results: In primary HSNEC, IL-8 mRNA levels decreased dose dependently in the range of 10-50 μM of AC with an eightfold decrease at 50 μM. In addition, a 125-fold decrease at 50 μM for IL-8 protein was observed. HBD-2 mRNA decreased twofold and HBD-2 protein decreased fourfold at 50 μM of AC in primary HSNEC. However, differentiated HSNEC showed a marginal decrease in a dose-dependent manner for both IL-8 and HBD-2 within the range of 10-50 μM of AC. There was no oxidative stress observed over this range of AC concentration. Conclusion: The tobacco smoke component AC has the capacity to suppress the inflammatory and innate immune function of sinonasal eoithelial cells. Whether this effect contributes to the negative clinical impact of smoking on CRS outcomes merits additional investigation.

Original languageEnglish (US)
Pages (from-to)658-663
Number of pages6
JournalAmerican Journal of Rhinology
Volume21
Issue number6
DOIs
StatePublished - Nov 2007

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Acrolein
Interleukin-8
Smoke
Tobacco Products
Epithelial Cells
Oxidative Stress
Gene Expression
Messenger RNA
human DEFB4A protein
Tobacco Use
Tobacco
Glutathione
Real-Time Polymerase Chain Reaction
Proteins
Smoking
Enzyme-Linked Immunosorbent Assay
Macrophages

Keywords

  • Acrolein
  • Defensin
  • Epithelial
  • IL-8
  • Immunity
  • Innate
  • Nasal
  • Rhinosinusitis
  • Tobacco

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

@article{0cf9648349df4906b24aa631604e614b,
title = "The cigarette smoke component acrolein inhibits expression of the innate immune components IL-8 and human beta-defensin 2 by sinonasal epithelial cells",
abstract = "Background: Tobacco use is associated with poorer outcomes of medical and surgical therapy for chronic rhinosinusitis (CRS), although the underlying mechanism is unknown. Acrolein (AC) is a major component of cigarette smoke that has been shown to suppress innate immune gene expression by human bronchial epithelial cells and murine macrophages. In this study, we explore whether exposure of human sinonasal epithelial cells (HSNECs) to AC similarly reduces their innate immune gene expression. Methods: Primary HSNECs from CRS patients were grown in culture, either differentiated or submerged. HSNECs were treated for 30 minutes with 0-50 μM of AC and were subsequently analyzed by real-time polymerase chain reaction and ELISA to determine IL-8 and human beta-defensin (HBD) 2 expression. Total glutathione was measured to see the oxidative stress within the treatment range. Results: In primary HSNEC, IL-8 mRNA levels decreased dose dependently in the range of 10-50 μM of AC with an eightfold decrease at 50 μM. In addition, a 125-fold decrease at 50 μM for IL-8 protein was observed. HBD-2 mRNA decreased twofold and HBD-2 protein decreased fourfold at 50 μM of AC in primary HSNEC. However, differentiated HSNEC showed a marginal decrease in a dose-dependent manner for both IL-8 and HBD-2 within the range of 10-50 μM of AC. There was no oxidative stress observed over this range of AC concentration. Conclusion: The tobacco smoke component AC has the capacity to suppress the inflammatory and innate immune function of sinonasal eoithelial cells. Whether this effect contributes to the negative clinical impact of smoking on CRS outcomes merits additional investigation.",
keywords = "Acrolein, Defensin, Epithelial, IL-8, Immunity, Innate, Nasal, Rhinosinusitis, Tobacco",
author = "Won, {Kyung Lee} and Murugappan Ramanathan and Spannhake, {Ernst W} and Lane, {Andrew P}",
year = "2007",
month = "11",
doi = "10.2500/ajr.2007.21.3094",
language = "English (US)",
volume = "21",
pages = "658--663",
journal = "American Journal of Rhinology and Allergy",
issn = "1945-8924",
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number = "6",

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TY - JOUR

T1 - The cigarette smoke component acrolein inhibits expression of the innate immune components IL-8 and human beta-defensin 2 by sinonasal epithelial cells

AU - Won, Kyung Lee

AU - Ramanathan, Murugappan

AU - Spannhake, Ernst W

AU - Lane, Andrew P

PY - 2007/11

Y1 - 2007/11

N2 - Background: Tobacco use is associated with poorer outcomes of medical and surgical therapy for chronic rhinosinusitis (CRS), although the underlying mechanism is unknown. Acrolein (AC) is a major component of cigarette smoke that has been shown to suppress innate immune gene expression by human bronchial epithelial cells and murine macrophages. In this study, we explore whether exposure of human sinonasal epithelial cells (HSNECs) to AC similarly reduces their innate immune gene expression. Methods: Primary HSNECs from CRS patients were grown in culture, either differentiated or submerged. HSNECs were treated for 30 minutes with 0-50 μM of AC and were subsequently analyzed by real-time polymerase chain reaction and ELISA to determine IL-8 and human beta-defensin (HBD) 2 expression. Total glutathione was measured to see the oxidative stress within the treatment range. Results: In primary HSNEC, IL-8 mRNA levels decreased dose dependently in the range of 10-50 μM of AC with an eightfold decrease at 50 μM. In addition, a 125-fold decrease at 50 μM for IL-8 protein was observed. HBD-2 mRNA decreased twofold and HBD-2 protein decreased fourfold at 50 μM of AC in primary HSNEC. However, differentiated HSNEC showed a marginal decrease in a dose-dependent manner for both IL-8 and HBD-2 within the range of 10-50 μM of AC. There was no oxidative stress observed over this range of AC concentration. Conclusion: The tobacco smoke component AC has the capacity to suppress the inflammatory and innate immune function of sinonasal eoithelial cells. Whether this effect contributes to the negative clinical impact of smoking on CRS outcomes merits additional investigation.

AB - Background: Tobacco use is associated with poorer outcomes of medical and surgical therapy for chronic rhinosinusitis (CRS), although the underlying mechanism is unknown. Acrolein (AC) is a major component of cigarette smoke that has been shown to suppress innate immune gene expression by human bronchial epithelial cells and murine macrophages. In this study, we explore whether exposure of human sinonasal epithelial cells (HSNECs) to AC similarly reduces their innate immune gene expression. Methods: Primary HSNECs from CRS patients were grown in culture, either differentiated or submerged. HSNECs were treated for 30 minutes with 0-50 μM of AC and were subsequently analyzed by real-time polymerase chain reaction and ELISA to determine IL-8 and human beta-defensin (HBD) 2 expression. Total glutathione was measured to see the oxidative stress within the treatment range. Results: In primary HSNEC, IL-8 mRNA levels decreased dose dependently in the range of 10-50 μM of AC with an eightfold decrease at 50 μM. In addition, a 125-fold decrease at 50 μM for IL-8 protein was observed. HBD-2 mRNA decreased twofold and HBD-2 protein decreased fourfold at 50 μM of AC in primary HSNEC. However, differentiated HSNEC showed a marginal decrease in a dose-dependent manner for both IL-8 and HBD-2 within the range of 10-50 μM of AC. There was no oxidative stress observed over this range of AC concentration. Conclusion: The tobacco smoke component AC has the capacity to suppress the inflammatory and innate immune function of sinonasal eoithelial cells. Whether this effect contributes to the negative clinical impact of smoking on CRS outcomes merits additional investigation.

KW - Acrolein

KW - Defensin

KW - Epithelial

KW - IL-8

KW - Immunity

KW - Innate

KW - Nasal

KW - Rhinosinusitis

KW - Tobacco

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U2 - 10.2500/ajr.2007.21.3094

DO - 10.2500/ajr.2007.21.3094

M3 - Article

VL - 21

SP - 658

EP - 663

JO - American Journal of Rhinology and Allergy

JF - American Journal of Rhinology and Allergy

SN - 1945-8924

IS - 6

ER -