Cigarette smoke inhibits human bronchial epithelial cell repair processes

H. Wang, Xiang-de Liu, T. Umino, C. M. Sköld, Y. Zhu, T. Kohyama, J. R. Spurzem, Debra Romberger, S. I. Rennard

Research output: Contribution to journalArticle

124 Citations (Scopus)

Abstract

By interfering with the ability of airway epithelial cells to support repair processes, cigarette smoke could contribute to alterations of airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). The current study assessed the ability of cigarette smoke extract (CSE) to alter human airway epithelial cell chemotaxis, proliferation, and contraction of three-dimensional collagen gels, a model of extracellular matrix remodeling. The volatile components contained in cigarette smoke, acetaldehyde and acrolein, were able to inhibit all three processes. Nonvolatile components contained within lyophilized CSE also inhibited chemotaxis but displayed no activity in the other two bioassays. CSE also inhibited the ability of airway epithelial cells to release transforming growth factor (TGF)-β and fibronectin. Exogenous fibronectin was unable to restore epithelial cell contraction of collagen gels. Exogenous TGF-β partially restored the ability of airway epithelial cells to contract collagen gels and to produce fibronectin. This supports a role for inhibition of TGF-β release in mediating the inhibitory effects of cigarette smoke. Taken together, the results of the current study suggest that epithelial cells present in the airways of smokers may be altered in their ability to support repair responses, which may contribute to architectural disruptions present in the airways in COPD associated with cigarette smoking.

Original languageEnglish (US)
Pages (from-to)772-779
Number of pages8
JournalAmerican journal of respiratory cell and molecular biology
Volume25
Issue number6
DOIs
StatePublished - Jan 1 2001

Fingerprint

Aptitude
Smoke
Tobacco Products
Repair
Epithelial Cells
Transforming Growth Factors
Fibronectins
Collagen
Gels
Pulmonary diseases
Chemotaxis
Chronic Obstructive Pulmonary Disease
Acrolein
Acetaldehyde
Bioassay
Biological Assay
Cell proliferation
Extracellular Matrix
Smoking
Cell Proliferation

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

Cite this

Cigarette smoke inhibits human bronchial epithelial cell repair processes. / Wang, H.; Liu, Xiang-de; Umino, T.; Sköld, C. M.; Zhu, Y.; Kohyama, T.; Spurzem, J. R.; Romberger, Debra; Rennard, S. I.

In: American journal of respiratory cell and molecular biology, Vol. 25, No. 6, 01.01.2001, p. 772-779.

Research output: Contribution to journalArticle

Wang, H. ; Liu, Xiang-de ; Umino, T. ; Sköld, C. M. ; Zhu, Y. ; Kohyama, T. ; Spurzem, J. R. ; Romberger, Debra ; Rennard, S. I. / Cigarette smoke inhibits human bronchial epithelial cell repair processes. In: American journal of respiratory cell and molecular biology. 2001 ; Vol. 25, No. 6. pp. 772-779.
@article{c0f437e3d5a8422abdbdb00ec05646fd,
title = "Cigarette smoke inhibits human bronchial epithelial cell repair processes",
abstract = "By interfering with the ability of airway epithelial cells to support repair processes, cigarette smoke could contribute to alterations of airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). The current study assessed the ability of cigarette smoke extract (CSE) to alter human airway epithelial cell chemotaxis, proliferation, and contraction of three-dimensional collagen gels, a model of extracellular matrix remodeling. The volatile components contained in cigarette smoke, acetaldehyde and acrolein, were able to inhibit all three processes. Nonvolatile components contained within lyophilized CSE also inhibited chemotaxis but displayed no activity in the other two bioassays. CSE also inhibited the ability of airway epithelial cells to release transforming growth factor (TGF)-β and fibronectin. Exogenous fibronectin was unable to restore epithelial cell contraction of collagen gels. Exogenous TGF-β partially restored the ability of airway epithelial cells to contract collagen gels and to produce fibronectin. This supports a role for inhibition of TGF-β release in mediating the inhibitory effects of cigarette smoke. Taken together, the results of the current study suggest that epithelial cells present in the airways of smokers may be altered in their ability to support repair responses, which may contribute to architectural disruptions present in the airways in COPD associated with cigarette smoking.",
author = "H. Wang and Xiang-de Liu and T. Umino and Sk{\"o}ld, {C. M.} and Y. Zhu and T. Kohyama and Spurzem, {J. R.} and Debra Romberger and Rennard, {S. I.}",
year = "2001",
month = "1",
day = "1",
doi = "10.1165/ajrcmb.25.6.4458",
language = "English (US)",
volume = "25",
pages = "772--779",
journal = "American Journal of Respiratory Cell and Molecular Biology",
issn = "1044-1549",
publisher = "American Thoracic Society",
number = "6",

}

TY - JOUR

T1 - Cigarette smoke inhibits human bronchial epithelial cell repair processes

AU - Wang, H.

AU - Liu, Xiang-de

AU - Umino, T.

AU - Sköld, C. M.

AU - Zhu, Y.

AU - Kohyama, T.

AU - Spurzem, J. R.

AU - Romberger, Debra

AU - Rennard, S. I.

PY - 2001/1/1

Y1 - 2001/1/1

N2 - By interfering with the ability of airway epithelial cells to support repair processes, cigarette smoke could contribute to alterations of airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). The current study assessed the ability of cigarette smoke extract (CSE) to alter human airway epithelial cell chemotaxis, proliferation, and contraction of three-dimensional collagen gels, a model of extracellular matrix remodeling. The volatile components contained in cigarette smoke, acetaldehyde and acrolein, were able to inhibit all three processes. Nonvolatile components contained within lyophilized CSE also inhibited chemotaxis but displayed no activity in the other two bioassays. CSE also inhibited the ability of airway epithelial cells to release transforming growth factor (TGF)-β and fibronectin. Exogenous fibronectin was unable to restore epithelial cell contraction of collagen gels. Exogenous TGF-β partially restored the ability of airway epithelial cells to contract collagen gels and to produce fibronectin. This supports a role for inhibition of TGF-β release in mediating the inhibitory effects of cigarette smoke. Taken together, the results of the current study suggest that epithelial cells present in the airways of smokers may be altered in their ability to support repair responses, which may contribute to architectural disruptions present in the airways in COPD associated with cigarette smoking.

AB - By interfering with the ability of airway epithelial cells to support repair processes, cigarette smoke could contribute to alterations of airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). The current study assessed the ability of cigarette smoke extract (CSE) to alter human airway epithelial cell chemotaxis, proliferation, and contraction of three-dimensional collagen gels, a model of extracellular matrix remodeling. The volatile components contained in cigarette smoke, acetaldehyde and acrolein, were able to inhibit all three processes. Nonvolatile components contained within lyophilized CSE also inhibited chemotaxis but displayed no activity in the other two bioassays. CSE also inhibited the ability of airway epithelial cells to release transforming growth factor (TGF)-β and fibronectin. Exogenous fibronectin was unable to restore epithelial cell contraction of collagen gels. Exogenous TGF-β partially restored the ability of airway epithelial cells to contract collagen gels and to produce fibronectin. This supports a role for inhibition of TGF-β release in mediating the inhibitory effects of cigarette smoke. Taken together, the results of the current study suggest that epithelial cells present in the airways of smokers may be altered in their ability to support repair responses, which may contribute to architectural disruptions present in the airways in COPD associated with cigarette smoking.

UR - http://www.scopus.com/inward/record.url?scp=0035198133&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035198133&partnerID=8YFLogxK

U2 - 10.1165/ajrcmb.25.6.4458

DO - 10.1165/ajrcmb.25.6.4458

M3 - Article

C2 - 11726404

AN - SCOPUS:0035198133

VL - 25

SP - 772

EP - 779

JO - American Journal of Respiratory Cell and Molecular Biology

JF - American Journal of Respiratory Cell and Molecular Biology

SN - 1044-1549

IS - 6

ER -