Evidence map›Paper›PMID 23632328›Full record

ArticleMucosal immunology2014

Lung epithelial cells are essential effectors of inducible resistance to pneumonia.

J O Cleaver, D You, D R Michaud, F A Guzmán Pruneda, M M Leiva Juarez, J Zhang, P M Weill, R Adachi, L Gong, S J Moghaddam and 3 more

Abstract read
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
–field-weighted citation impact
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

62 citing papers in PubMed.

  1. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Epithelial STAT3: A New Twist in Inducible Antimicrobial Resistance.American journal of respiratory cell and molecular biology · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Response of Lung Microbiota to Changes of Pulmonary Innate Immunity under Healthy Conditions.American journal of respiratory and critical care medicine · 2022
    Article

2 more citing papers are in PubMed but not listed here.

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

13 authors.

J O CleaverDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
D YouDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
D R MichaudDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
F A Guzmán Pruneda1] Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA [2] Tecnológico de Monterrey School of Medicine, Monterrey, Nuevo León, Mexico.
M M Leiva JuarezTecnológico de Monterrey School of Medicine, Monterrey, Nuevo León, Mexico.
J ZhangDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
P M WeillDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
R Adachi1] Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA [2] Center for Infectious and Inflammatory Disease, Institute of Biosciences and Technology, Texas A & M Health Science Center, Houston, Texas, USA.
L GongDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
S J Moghaddam1] Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA [2] Center for Infectious and Inflammatory Disease, Institute of Biosciences and Technology, Texas A & M Health Science Center, Houston, Texas, USA.
M E PoynterDivision of Pulmonary Disease and Critical Care, University of Vermont College of Medicine, Burlington, Vermont, USA.
M J Tuvim1] Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA [2] Center for Infectious and Inflammatory Disease, Institute of Biosciences and Technology, Texas A & M Health Science Center, Houston, Texas, USA.
S E Evans1] Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA [2] Center for Infectious and Inflammatory Disease, Institute of Biosciences and Technology, Texas A & M Health Science Center, Houston, Texas, USA [3] University of Texas Graduate School of Biomedical Science, Houston, Texas, USA.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KONOPLEVA, MARINA Y · 2003 to 2023
$43.7M
BINDING OF BACTERIA TO FIBRONECTIN AN FIBRINOGENR01AI020624 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HOOK, AXEL MAGNUS · 1985 to 2020
$9.7M
Inducible epithelial antiviral resistance to prevent asthmaDP2HL123229 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI EVANS, SCOTT E. · 2013 to 2013
$2.4M
Stimulated Innate Resistance of the Lungs to Bioterror pathogensU01AI082226 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI HOOK, AXEL MAGNUS · 2009 to 2013
$2.2M
Epithelial mechanisms of inducible resistance to AML-associated pneumoniaR01HL117976 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI EVANS, SCOTT E. · 2014 to 2018
$2.0M
Serum Amyloid A3 in Allergic Asthma: An Endogenous Mediator of Disease SeverityR01HL107291 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI POYNTER, MATTHEW E · 2012 to 2015
$1.5M
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA100632NHLBI NIH HHS DP2 HL123229NHLBI NIH HHS R01 HL107291NHLBI NIH HHS R01 HL117976NIAID NIH HHS R01 AI020624NIAID NIH HHS U01 AI082226NIAID NIH HHS U01 AI82226
6 · The paper itself

Abstract

Infectious pneumonias are the leading cause of death worldwide, particularly among immunocompromised patients. Therapeutic stimulation of the lungs' intrinsic defenses with a unique combination of inhaled Toll-like receptor (TLR) agonists broadly protects mice against otherwise lethal pneumonias. As the survival benefit persists despite cytotoxic chemotherapy-related neutropenia, the cells required for protection were investigated. The inducibility of resistance was tested in mice with deficiencies of leukocyte lineages due to genetic deletions and in wild-type mice with leukocyte populations significantly reduced by antibodies or toxins. Surprisingly, these serial reductions in leukocyte lineages did not appreciably impair inducible resistance, but targeted disruption of TLR signaling in the lung epithelium resulted in complete abrogation of the protective effect. Isolated lung epithelial cells were also induced to kill pathogens in the absence of leukocytes. Proteomic and gene expression analyses of isolated epithelial cells and whole lungs revealed highly congruent antimicrobial responses. Taken together, these data indicate that lung epithelial cells are necessary and sufficient effectors of inducible resistance. These findings challenge conventional paradigms about the role of epithelia in antimicrobial defense and offer a novel potential intervention to protect patients with impaired leukocyte-mediated immunity from fatal pneumonias.

Indexed as

Alveolar Epithelial CellsAnimalsDisease Models, AnimalDisease ResistanceLeukocytesLipopeptidesMiceMice, KnockoutPneumoniaSignal TransductionToll-Like ReceptorsLipopeptidesPam2CSK4 lipopeptideToll-Like Receptors

Identifiers

PMID23632328
PMCPMC3735803

What OpenQuestion holds

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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.