Evidence map›Paper›PMID 26066648›Full record

ArticlePloS one2015

Airway Surface Dehydration Aggravates Cigarette Smoke-Induced Hallmarks of COPD in Mice.

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 and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
  3. Article
  4. Chronic hyperglycemia aggravates lung function in aAmerican journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  5. Article
  6. Article
  7. Genetic Deletion ofInternational journal of molecular sciences · 2022
    Article
  8. Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  9. Article
  10. Article
  11. Trypsin-Like Proteases and Their Role in Muco-Obstructive Lung Diseases.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Cigarillos Compromise the Mucosal Barrier and Protein Expression in Airway Epithelia.American journal of respiratory cell and molecular biology · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Cigarette smoke modifies and inactivates SPLUNC1, leading to airway dehydration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Leen J M SeysLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Fien M VerhammeLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Lisa L DupontLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Elke DesauterLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Julia DuerrDepartment of Translational Pulmonology, Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), University of Heidelberg, Heidelberg, Germany.
Ayca Seyhan AgircanDepartment of Translational Pulmonology, Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), University of Heidelberg, Heidelberg, Germany.
Griet ConickxLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Guy F JoosLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Guy G BrusselleLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Marcus A MallDepartment of Translational Pulmonology, Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), University of Heidelberg, Heidelberg, Germany.
Ken R BrackeLaboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Ghent University Hospital · BEHeidelberg University · DEGerman Center for Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAirway 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.

objectiveWe 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).

methodsβENaC-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.

resultsAirway 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.

conclusionsWe conclude that airway surface dehydration is a risk factor that aggravates CS-induced hallmarks of COPD.

Indexed as

AnimalsCells, CulturedDehydrationEpithelial Sodium ChannelsMaleMiceMice, Inbred C57BLMucinsPulmonary Disease, Chronic ObstructiveRespiratory MucosaSmokingTobacco Smoke PollutionEpithelial Sodium ChannelsMucinsTobacco Smoke Pollution

Identifiers

PMID26066648
PMCPMC4466573
OpenAlexW2216185281

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.