Evidence map›Paper›PMID 22514650›Full record

ArticlePloS one2012

Differential requirement for c-Jun N-terminal kinase 1 in lung inflammation and host defense.

Jos Van der Velden, Yvonne M W Janssen-Heininger, Sivanarayna Mandalapu, Erich V Scheller, Jay K Kolls, John F Alcorn

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Biological sex influences immune response to influenza infection in juvenile outbred mice.American journal of physiology. Lung cellular and molecular physiology · 2026
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  5. Lnc90386 Sponges miR-33-5p to MediateFrontiers in immunology · 2022
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  14. POSH Regulates CD4+ T Cell Differentiation and Survival.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  15. A tale of two cytokines: IL-17 and IL-22 in asthma and infection.Expert review of respiratory medicine · 2014
    Review
  16. 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

6 authors at 3 institutions in 1 country.

Jos Van der VeldenDepartment of Pathology, University of Vermont, Burlington, Vermont, United States of America.
Yvonne M W Janssen-Heininger
Sivanarayna Mandalapu
Erich V Scheller
Jay K Kolls
John F Alcorn
Children's Hospital of Pittsburgh · USUniversity of Vermont · USRichard King Mellon Foundation · US

Funding

Th17 Cytokines and Lung ImmunityR37HL079142 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KOLLS, JAY K · 2010 to 2017
$3.6M
Epithelial JNK-TGFb1 Signaling Axis in Airway RemodelingR01HL085464 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI JANSSEN-HEININGER, YVONNE M. W. · 2008 to 2016
$3.0M
NHLBI NIH HHS R01 HL085464NHLBI NIH HHS R37 HL079142
6 · The paper itself

Abstract

The c-Jun N-terminal kinase (JNK) - 1 pathway has been implicated in the cellular response to stress in many tissues and models. JNK1 is known to play a role in a variety of signaling cascades, including those involved in lung disease pathogenesis. Recently, a role for JNK1 signaling in immune cell function has emerged. The goal of the present study was to determine the role of JNK1 in host defense against both bacterial and viral pneumonia, as well as the impact of JNK1 signaling on IL-17 mediated immunity. Wild type (WT) and JNK1 -/- mice were challenged with Escherichia coli, Staphylococcus aureus, or Influenza A. In addition, WT and JNK1 -/- mice and epithelial cells were stimulated with IL-17A. The impact of JNK1 deletion on pathogen clearance, inflammation, and histopathology was assessed. JNK1 was required for clearance of E. coli, inflammatory cell recruitment, and cytokine production. Interestingly, JNK1 deletion had only a small impact on the host response to S. aureus. JNK1 -/- mice had decreased Influenza A burden in viral pneumonia, yet displayed worsened morbidity. Finally, JNK1 was required for IL-17A mediated induction of inflammatory cytokines and antimicrobial peptides both in epithelial cells and the lung. These data identify JNK1 as an important signaling molecule in host defense and demonstrate a pathogen specific role in disease. Manipulation of the JNK1 pathway may represent a novel therapeutic target in pneumonia.

Indexed as

AnimalsCells, CulturedInterleukin-17LungMiceMice, KnockoutMitogen-Activated Protein Kinase 8PneumoniaSignal TransductionStaphylococcus aureusInterleukin-17Mitogen-Activated Protein Kinase 8

Identifiers

PMID22514650
PMCPMC3326034
OpenAlexW2071183881

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.