Advanced search
1 file | 3.71 MB Add to list

Airway surface dehydration aggravates cigarette smoke-induced hallmarks of COPD in mice

Leen Seys (UGent) , Fien Verhamme (UGent) , Lisa Dupont (UGent) , Elke Desauter, Julia Duerr, Ayca Seyhan Agircan, Griet Conickx (UGent) , Guy Joos (UGent) , Guy Brusselle (UGent) , Marcus A Mall, et al.
(2015) PLOS ONE. 10(6).
Author
Organization
Abstract
Introduction: Airway surface dehydration, caused by an imbalance between secretion and absorption of ions and fluid across the epithelium and/or increased epithelial mucin secretion, impairs mucociliary clearance. Recent evidence suggests that this mechanism may be implicated in chronic obstructive pulmonary disease (COPD). However, the role of airway surface dehydration in the pathogenesis of cigarette smoke (CS)-induced COPD remains unknown. Objective: We aimed to investigate in vivo the effect of airway surface dehydration on several CS-induced hallmarks of COPD in mice with airway-specific overexpression of the β-subunit of the epithelial Na+ channel (βENaC). Methods: βENaC-Tg mice and wild-type (WT) littermates were exposed to air or CS for 4 or 8 weeks. Pathological hallmarks of COPD, including goblet cell metaplasia, mucin expression, pulmonary inflammation, lymphoid follicles, emphysema and airway wall remodelling were determined and lung function was measured. Results: Airway surface dehydration in βENaC-Tg mice aggravated CS-induced airway inflammation, mucin expression and destruction of alveolar walls and accelerated the formation of pulmonary lymphoid follicles. Moreover, lung function measurements demonstrated an increased compliance and total lung capacity and a lower resistance and hysteresis in βENaC-Tg mice, compared to WT mice. CS exposure further altered lung function measurements. Conclusions: We conclude that airway surface dehydration is a risk factor that aggravates CS-induced hallmarks of COPD.
Keywords
CONDUCTANCE, CELL, HEALTH, INFLAMMATION, ANIMAL-MODELS, LUNG-DISEASE, CHRONIC-BRONCHITIS, INDUCED EMPHYSEMA, MUCUS CLEARANCE, OBSTRUCTIVE PULMONARY-DISEASE

Downloads

  • Seys LJ Airway Surface Dehydration.pdf
    • full text
    • |
    • open access
    • |
    • PDF
    • |
    • 3.71 MB

Citation

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

MLA
Seys, Leen et al. “Airway Surface Dehydration Aggravates Cigarette Smoke-induced Hallmarks of COPD in Mice.” PLOS ONE 10.6 (2015): n. pag. Print.
APA
Seys, L., Verhamme, F., Dupont, L., Desauter, E., Duerr, J., Agircan, A. S., Conickx, G., et al. (2015). Airway surface dehydration aggravates cigarette smoke-induced hallmarks of COPD in mice. PLOS ONE, 10(6).
Chicago author-date
Seys, Leen, Fien Verhamme, Lisa Dupont, Elke Desauter, Julia Duerr, Ayca Seyhan Agircan, Griet Conickx, et al. 2015. “Airway Surface Dehydration Aggravates Cigarette Smoke-induced Hallmarks of COPD in Mice.” Plos One 10 (6).
Chicago author-date (all authors)
Seys, Leen, Fien Verhamme, Lisa Dupont, Elke Desauter, Julia Duerr, Ayca Seyhan Agircan, Griet Conickx, Guy Joos, Guy Brusselle, Marcus A Mall, and Ken Bracke. 2015. “Airway Surface Dehydration Aggravates Cigarette Smoke-induced Hallmarks of COPD in Mice.” Plos One 10 (6).
Vancouver
1.
Seys L, Verhamme F, Dupont L, Desauter E, Duerr J, Agircan AS, et al. Airway surface dehydration aggravates cigarette smoke-induced hallmarks of COPD in mice. PLOS ONE. 2015;10(6).
IEEE
[1]
L. Seys et al., “Airway surface dehydration aggravates cigarette smoke-induced hallmarks of COPD in mice,” PLOS ONE, vol. 10, no. 6, 2015.
@article{6907982,
  abstract     = {Introduction: Airway surface dehydration, caused by an imbalance between secretion and absorption of ions and fluid across the epithelium and/or increased epithelial mucin secretion, impairs mucociliary clearance. Recent evidence suggests that this mechanism may be implicated in chronic obstructive pulmonary disease (COPD). However, the role of airway surface dehydration in the pathogenesis of cigarette smoke (CS)-induced COPD remains unknown.
Objective: We aimed to investigate in vivo the effect of airway surface dehydration on several CS-induced hallmarks of COPD in mice with airway-specific overexpression of the β-subunit of the epithelial Na+ channel (βENaC).
Methods: βENaC-Tg mice and wild-type (WT) littermates were exposed to air or CS for 4 or 8 weeks. Pathological hallmarks of COPD, including goblet cell metaplasia, mucin expression, pulmonary inflammation, lymphoid follicles, emphysema and airway wall remodelling were determined and lung function was measured.
Results: Airway surface dehydration in βENaC-Tg mice aggravated CS-induced airway inflammation, mucin expression and destruction of alveolar walls and accelerated the formation of pulmonary lymphoid follicles. Moreover, lung function measurements demonstrated an increased compliance and total lung capacity and a lower resistance and hysteresis in βENaC-Tg mice, compared to WT mice. CS exposure further altered lung function measurements.
Conclusions: We conclude that airway surface dehydration is a risk factor that aggravates CS-induced hallmarks of COPD.},
  articleno    = {e0129897},
  author       = {Seys, Leen and Verhamme, Fien and Dupont, Lisa and Desauter, Elke and Duerr, Julia and Agircan, Ayca Seyhan and Conickx, Griet and Joos, Guy and Brusselle, Guy and Mall, Marcus A and Bracke, Ken},
  issn         = {1932-6203},
  journal      = {PLOS ONE},
  keywords     = {CONDUCTANCE,CELL,HEALTH,INFLAMMATION,ANIMAL-MODELS,LUNG-DISEASE,CHRONIC-BRONCHITIS,INDUCED EMPHYSEMA,MUCUS CLEARANCE,OBSTRUCTIVE PULMONARY-DISEASE},
  language     = {eng},
  number       = {6},
  pages        = {18},
  title        = {Airway surface dehydration aggravates cigarette smoke-induced hallmarks of COPD in mice},
  url          = {http://dx.doi.org/10.1371/journal.pone.0129897},
  volume       = {10},
  year         = {2015},
}

Altmetric
View in Altmetric
Web of Science
Times cited: