Evidence map›Paper›PMID 26121027›Full record

ArticleAmerican journal of respiratory cell and molecular biology2016

Neonatal Pulmonary Macrophage Depletion Coupled to Defective Mucus Clearance Increases Susceptibility to Pneumonia and Alters Pulmonary Immune Responses.

Yogesh Saini, Kristen J Wilkinson, Kristy A Terrell, Kimberlie A Burns, Alessandra Livraghi-Butrico, Claire M Doerschuk, Wanda K O'Neal, Richard C Boucher

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.American journal of respiratory cell and molecular biology · 2026
    Article
  2. Article
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  7. Induction of whole-body gene deletionFrontiers in pharmacology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Enhanced epithelial sodium channel activity in neonatal Scnn1b mouse lung attenuates high oxygen-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  13. Article
  14. Ablation of IL-33 SuppressesJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  15. Review
  16. Article
  17. Pneumonia.Seminars in fetal & neonatal medicine · 2017
    Review
  18. Review
  19. 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

8 authors at 1 institution in 1 country.

Yogesh Saini1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
Kristen J Wilkinson1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
Kristy A Terrell1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
Kimberlie A Burns1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
Alessandra Livraghi-Butrico1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
Claire M Doerschuk1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
Wanda K O'Neal1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
Richard C Boucher1 Marsico Lung Institute/University of North Carolina Cystic Fibrosis Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and.
University of North Carolina at Chapel Hill · US

Funding

Vector CoreP30DK065988 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Richard Charles Boucher, Martina Gentzsch · 2004 to 2026
$26.5M
The Biophysics of Mucus Hydration and Adhesion/CohesionP01HL108808 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PEDEN, DAVID B. · 2012 to 2021
$23.9M
THE BIOLOGY OF MUCUS AND MUCUS PLAQUES ON CF AIRWAYSP50HL060280 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CHUA, MICHAEL · 1998 to 2007
$14.0M
Mucus Adhesion to Epithelial Cells and its Mobilization in COPD and CFP50HL107168 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BOUCHER, RICHARD CHARLES, DOERSCHUK, CLAIRE M · 2011 to 2012
$885k
NHLBI NIH HHS P01 HL108808NHLBI NIH HHS P01HL108808NHLBI NIH HHS P50 HL060280NHLBI NIH HHS P50 HL107168NHLBI NIH HHS P50HL107168NIDDK NIH HHS P30 DK065988
6 · The paper itself

Abstract

Resident immune cells (e.g., macrophages [MΦs]) and airway mucus clearance both contribute to a healthy lung environment. To investigate interactions between pulmonary MΦ function and defective mucus clearance, a genetic model of lysozyme M (LysM) promoter-mediated MΦ depletion was generated, characterized, and crossed with the sodium channel β subunit transgenic (Scnn1b-Tg) mouse model of defective mucus clearance. Diphtheria toxin A-mediated depletion of LysM(+) pulmonary MΦs in wild-type mice with normal mucus clearance resulted in lethal pneumonia in 24% of neonates. The pneumonias were dominated by Pasteurella pneumotropica and accompanied by emaciation, neutrophilic inflammation, and elevated Th1 cytokines. The incidence of emaciation and pneumonia reached 51% when LysM(+) MΦ depletion was superimposed on the airway mucus clearance defect of Scnn1b-Tg mice. In LysM(+) MΦ-depleted Scnn1b-Tg mice, pneumonias were associated with a broader spectrum of bacterial species and a significant reduction in airway mucus plugging. Bacterial burden (CFUs) was comparable between Scnn1b-Tg and nonpneumonic LysM(+) MΦ-depleted Scnn1b-Tg mice. However, the nonpneumonic LysM(+) MΦ-depleted Scnn1b-Tg mice exhibited increased airway inflammation, the presence of neutrophilic infiltration, and increased levels of inflammatory cytokines in bronchoalveolar lavage fluid compared with Scnn1b-Tg mice. Collectively, these data identify key MΦ-mucus clearance interactions with respect to both infectious and inflammatory components of muco-obstructive lung disease.

Indexed as

Mucociliary ClearanceAnimalsAnimals, NewbornCytokinesDiphtheria ToxinDisease Models, AnimalEpithelial Sodium ChannelsGenetic Predisposition to DiseaseInflammation MediatorsLuminescent ProteinsLungMacrophagesMice, Inbred C57BLMice, TransgenicMuramidasePasteurella InfectionsCytokinesDiphtheria Toxindiphtheria toxin fragment AEpithelial Sodium ChannelsInflammation MediatorsLuminescent ProteinsMuramidasePeptide Fragmentsairway inflammationairway mucus obstructionalveolar macrophagesmacrophage depletionsodium channel β subunit transgenic mice

Identifiers

PMID26121027
PMCPMC4821038
OpenAlexW2180185118

What OpenQuestion holds

Textmetadata
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.