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Verfasst von:Seys, Leen J.M. [VerfasserIn]   i
 Verhamme, Fien M. [VerfasserIn]   i
 Dupont, Lisa L. [VerfasserIn]   i
 Desauter, Elke [VerfasserIn]   i
 Dürr, Julia [VerfasserIn]   i
 Seyhan Agircan, Ayca [VerfasserIn]   i
 Conickx, Griet [VerfasserIn]   i
 Joos, Guy F. [VerfasserIn]   i
 Brusselle, Guy G. [VerfasserIn]   i
 Mall, Marcus A. [VerfasserIn]   i
 Bracke, Ken R. [VerfasserIn]   i
Titel:Airway surface dehydration aggravates cigarette smoke-induced hallmarks of COPD in mice
Verf.angabe:Leen J.M. Seys, Fien M. Verhamme, Lisa L. Dupont, Elke Desauter, Julia Duerr, Ayca Seyhan Agircan, Griet Conickx, Guy F. Joos, Guy G. Brusselle, Marcus A. Mall, Ken R. Bracke
E-Jahr:2015
Jahr:June 12, 2015
Fussnoten:Gesehen am 17.06.2020
Titel Quelle:Enthalten in: PLOS ONE
Ort Quelle:San Francisco, California, US : PLOS, 2006
Jahr Quelle:2015
Band/Heft Quelle:10(2015,6) Artikel-Nummer e0129897,18 Seiten
ISSN Quelle:1932-6203
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.
DOI:doi:10.1371/journal.pone.0129897
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1371/journal.pone.0129897
 Volltext: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0129897
 DOI: https://doi.org/10.1371/journal.pone.0129897
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Chronic obstructive pulmonary disease
 Dehydration (medicine)
 Emphysema
 Inflammation
 Lymphoid follicles
 Mucin
 Mucus
 Pulmonary function
K10plus-PPN:1700717375
Verknüpfungen:→ Zeitschrift

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