Advanced search
1 file | 1.13 MB Add to list

Enhanced pulmonary leptin expression in patients with severe COPD and asymptomatic smokers

(2009) Thorax. 64(1). p.26-32
Author
Organization
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is characterised by an abnormal inflammatory reaction of the lungs involving activation of epithelial cells. Leptin is a pleiotropic cytokine important in the regulation of immune responses via its functional receptor Ob-Rb. This study was undertaken to test the hypothesis that severe COPD is associated with increased leptin expression in epithelial cells. Methods: Immunohistochemistry for leptin was performed on peripheral lung specimens from 20 patients with COPD (GOLD stage 4), 14 asymptomatic ex-smokers and 13 never smokers. Leptin and Ob-Rb mRNA expression were determined by rtPCR in cultured primary bronchial epithelial cells and primary type II pneumocytes. NCI-H292 and A549 cell lines were used to study functional activation of leptin signalling. Results: Leptin immunoreactivity in lung tissue was observed in bronchial epithelial cells, type II pneumocytes, macrophages (tissue/alveolar) and interstitial lymphocytic infiltrates. rtPCR analysis confirmed pulmonary leptin and Ob-Rb mRNA expression in primary bronchial epithelial cells and pneumocytes. Leptin- expressing bronchial epithelial cells and alveolar macrophages were markedly higher in patients with severe COPD and ex-smokers than in never smokers (p<0.02). Exposure of cultured primary bronchial epithelial cells to smoke resulted in increased expression of both leptin and Ob-Rb (p<0.05). Leptin induced phosphorylation of STAT3 in both NCI-H292 and A549 cells. Conclusions: Leptin expression is increased in bronchial epithelial cells and alveolar macrophages of ex-smokers with or without severe COPD compared with never smokers. A functional leptin signalling pathway is present in lung epithelial cells.
Keywords
starvation, pneumonia, activation, proliferation, lung, receptor, disease, host-defense, Epithelial cells, T-lymphocytes

Downloads

  • (...).pdf
    • full text
    • |
    • UGent only
    • |
    • PDF
    • |
    • 1.13 MB

Citation

Please use this url to cite or link to this publication:

MLA
Vernooy, JHJ, et al. “Enhanced Pulmonary Leptin Expression in Patients with Severe COPD and Asymptomatic Smokers.” Thorax, vol. 64, no. 1, BMJ Publishing Group, 2009, pp. 26–32, doi:10.1136/thx.2007.085423.
APA
Vernooy, J., Drummen, N., Van Suylen, R., Cloots, R., Moller, G., Bracke, K., … Wouters, E. (2009). Enhanced pulmonary leptin expression in patients with severe COPD and asymptomatic smokers. Thorax, 64(1), 26–32. https://doi.org/10.1136/thx.2007.085423
Chicago author-date
Vernooy, JHJ, NEA Drummen, RJ Van Suylen, RHE Cloots, GM Moller, Ken Bracke, S Zuyderduyn, et al. 2009. “Enhanced Pulmonary Leptin Expression in Patients with Severe COPD and Asymptomatic Smokers.” Thorax 64 (1): 26–32. https://doi.org/10.1136/thx.2007.085423.
Chicago author-date (all authors)
Vernooy, JHJ, NEA Drummen, RJ Van Suylen, RHE Cloots, GM Moller, Ken Bracke, S Zuyderduyn, MA Dentener, Guy Brusselle, PS Hiemstra, and EFM Wouters. 2009. “Enhanced Pulmonary Leptin Expression in Patients with Severe COPD and Asymptomatic Smokers.” Thorax 64 (1): 26–32. doi:10.1136/thx.2007.085423.
Vancouver
1.
Vernooy J, Drummen N, Van Suylen R, Cloots R, Moller G, Bracke K, et al. Enhanced pulmonary leptin expression in patients with severe COPD and asymptomatic smokers. Thorax. 2009;64(1):26–32.
IEEE
[1]
J. Vernooy et al., “Enhanced pulmonary leptin expression in patients with severe COPD and asymptomatic smokers,” Thorax, vol. 64, no. 1, pp. 26–32, 2009.
@article{537346,
  abstract     = {{Background: Chronic obstructive pulmonary disease (COPD) is characterised by an abnormal inflammatory reaction of the lungs involving activation of epithelial cells. Leptin is a pleiotropic cytokine important in the regulation of immune responses via its functional receptor Ob-Rb. This study was undertaken to test the hypothesis that severe COPD is associated with increased leptin expression in epithelial cells.
Methods: Immunohistochemistry for leptin was performed on peripheral lung specimens from 20 patients with COPD (GOLD stage 4), 14 asymptomatic ex-smokers and 13 never smokers. Leptin and Ob-Rb mRNA expression were determined by rtPCR in cultured primary bronchial epithelial cells and primary type II pneumocytes. NCI-H292 and A549 cell lines were used to study functional activation of leptin signalling.

Results: Leptin immunoreactivity in lung tissue was observed in bronchial epithelial cells, type II pneumocytes, macrophages (tissue/alveolar) and interstitial lymphocytic infiltrates. rtPCR analysis confirmed pulmonary leptin and Ob-Rb mRNA expression in primary bronchial epithelial cells and pneumocytes. Leptin- expressing bronchial epithelial cells and alveolar macrophages were markedly higher in patients with severe COPD and ex-smokers than in never smokers (p<0.02). Exposure of cultured primary bronchial epithelial cells to smoke resulted in increased expression of both leptin and Ob-Rb (p<0.05). Leptin induced phosphorylation of STAT3 in both NCI-H292 and A549 cells.

Conclusions: Leptin expression is increased in bronchial epithelial cells and alveolar macrophages of ex-smokers with or without severe COPD compared with never smokers. A functional leptin signalling pathway is present in lung epithelial cells.}},
  author       = {{Vernooy, JHJ and Drummen, NEA and Van Suylen, RJ and Cloots, RHE and Moller, GM and Bracke, Ken and Zuyderduyn, S and Dentener, MA and Brusselle, Guy and Hiemstra, PS and Wouters, EFM}},
  issn         = {{0040-6376}},
  journal      = {{Thorax}},
  keywords     = {{starvation,pneumonia,activation,proliferation,lung,receptor,disease,host-defense,Epithelial cells,T-lymphocytes}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{26--32}},
  publisher    = {{BMJ Publishing Group}},
  title        = {{Enhanced pulmonary leptin expression in patients with severe COPD and asymptomatic smokers}},
  url          = {{http://doi.org/10.1136/thx.2007.085423}},
  volume       = {{64}},
  year         = {{2009}},
}

Altmetric
View in Altmetric
Web of Science
Times cited: