Evidence map›Paper›PMID 23187315›Full record

ArticleMucosal immunology2013

Detrimental role of the airway mucin Muc5ac during ventilator-induced lung injury.

M Koeppen, E N McNamee, K S Brodsky, C M Aherne, M Faigle, G P Downey, S P Colgan, C M Evans, D A Schwartz, H K Eltzschig

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing 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

55 citing papers in PubMed, 89 citations in OpenAlex.

  1. Mucins and Respiratory Virus Infection.Annual review of virology · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Normalization of Muc5b ameliorates airway mucus plugging during persistentAmerican journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Prevalence and Mechanisms of Mucus Accumulation in COVID-19 Lung Disease.American journal of respiratory and critical care medicine · 2022
    Article
  19. Review
  20. Review
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

10 authors at 3 institutions in 2 countries.

M KoeppenMucosal Inflammation Program, Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
E N McNamee
K S Brodsky
C M Aherne
M Faigle
G P Downey
S P Colgan
C M Evans
D A Schwartz
H K Eltzschig
University of Colorado Anschutz Medical Campus · USNational Jewish Health · USUniversity Children's Hospital Tübingen · DE

Funding

Hypoxia, HIF, and Mucosal InflammationR37DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2010 to 2019
$4.1M
Extracellular Adenosine During Ventilator Induced Lung InjuryR01HL092188 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ELTZSCHIG, HOLGER K. · 2009 to 2013
$2.1M
Focal Adhesion Modulation of IL-1 Signaling: Importance in Pulmonary FibrosisR01HL090669 · NHLBI · NATIONAL JEWISH HEALTH · PI DOWNEY, GREGORY PAUL · 2008 to 2011
$1.8M
Hypoxia Inducible Factor in Acute Lung InjuryR01HL098294 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ELTZSCHIG, HOLGER K. · 2011 to 2014
$1.6M
Alternative Mechanisms of Adenosine Receptor ActivationR01DK083385 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI ELTZSCHIG, HOLGER K. · 2010 to 2013
$1.2M
NHLBI NIH HHS R01 HL090669NHLBI NIH HHS R01-HL0921NHLBI NIH HHS R01 HL092188NHLBI NIH HHS R01 HL098294NHLBI NIH HHS R01HL098294NIDDK NIH HHS R01 DK083385NIDDK NIH HHS R01-DK083385NIDDK NIH HHS R37 DK050189
6 · The paper itself

Abstract

Acute lung injury (ALI) is associated with high morbidity and mortality in critically ill patients. At present, the functional contribution of airway mucins to ALI is unknown. We hypothesized that excessive mucus production could be detrimental during lung injury. Initial transcriptional profiling of airway mucins revealed a selective and robust induction of MUC5AC upon cyclic mechanical stretch exposure of pulmonary epithelia (Calu-3). Additional studies confirmed time- and stretch-dose-dependent induction of MUC5AC transcript or protein during cyclic mechanical stretch exposure in vitro or during ventilator-induced lung injury in vivo. Patients suffering from ALI showed a 58-fold increase in MUC5AC protein in their bronchoalveolar lavage. Studies of the MUC5AC promoter implicated nuclear factor κB in Muc5ac induction during ALI. Moreover, mice with gene-targeted deletion of Muc5ac⁻/⁻ experience attenuated lung inflammation and pulmonary edema during injurious ventilation. We observed that neutrophil trafficking into the lungs of Muc5ac⁻/⁻ mice was selectively attenuated. This implicates that endogenous Muc5ac production enhances pulmonary neutrophil trafficking during lung injury. Together, these studies reveal a detrimental role for endogenous Muc5ac production during ALI and suggest pharmacological strategies to dampen mucin production in the treatment of lung injury.

Indexed as

AnimalsChemotaxis, LeukocyteDisease Models, AnimalGene DeletionGene Expression ProfilingGene Expression RegulationHumansMiceMice, KnockoutMucin 5ACNeutrophil InfiltrationNeutrophilsNF-kappa BPneumoniaRespiratory MucosaStress, MechanicalMucin 5ACNF-kappa B

Identifiers

PMID23187315
PMCPMC3890100
OpenAlexW2078908709

What OpenQuestion holds

Textmetadata
LicenceTDM
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.