Evidence map›Paper›PMID 24470495›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

G-CSF drives a posttraumatic immune program that protects the host from infection.

Jason C Gardner, John G Noel, Nikolaos M Nikolaidis, Rebekah Karns, Bruce J Aronow, Cora K Ogle, Francis X McCormack

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.1field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. IL-1/MyD88-Dependent G-CSF and IL-6 Secretion Mediates Postburn Anemia.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
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  10. Enhancement of cellular activity in hyperglycemic mice dermal wounds dressed with chitosan-alginate membranes.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
  11. Article
  12. Article
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  15. Article
  16. Article
  17. Article
  18. STAT3 signaling in immunity.Cytokine & growth factor reviews · 2016
    Review
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  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

7 authors at 3 institutions in 1 country.

Jason C GardnerDivision of Pulmonary, Critical Care and Sleep Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267;
John G Noel
Nikolaos M Nikolaidis
Rebekah Karns
Bruce J Aronow
Cora K Ogle
Francis X McCormack
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USShriners Hospitals for Children - Cincinnati · US

Funding

Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., TSEVAT, JOEL · 2012 to 2014
$9.9M
Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
NCATS NIH HHS 8 UL1 TR000077-05NCATS NIH HHS UL1 TR000077NIDDK NIH HHS P30 DK090971
6 · The paper itself

Abstract

Traumatic injury is generally considered to have a suppressive effect on the immune system, resulting in increased susceptibility to infection. Paradoxically, we found that thermal injury to the skin induced a robust time-dependent protection of mice from a lethal Klebsiella pneumoniae pulmonary challenge. The protective response was neutrophil dependent and temporally associated with a systemic increase in neutrophils resulting from a reprioritization of hematopoiesis toward myeloid lineages. A prominent and specific activation of STAT3 in the bone marrow preceded the myeloid shift in that compartment, in association with durable increases in STAT3 activating serum cytokines G-CSF and IL-6. Neutralization of the postburn increase in serum G-CSF largely blocked STAT3 activation in marrow cells, reversing the hematopoietic changes and systemic neutrophilia. Daily administration of rG-CSF was sufficient to recapitulate the changes induced by injury including hematopoietic reprioritization and protection from pulmonary challenge with K. pneumoniae. Analysis of posttraumatic gene expression patterns in humans reveals that they are also consistent with a role for G-CSF as a switch that activates innate immune responses and suppresses adaptive immune responses. Our findings suggest that the G-CSF STAT3 axis constitutes a key protective mechanism induced by injury to reduce the risk for posttraumatic infection.

Indexed as

Adaptive ImmunityAnimalsBone Marrow CellsBurnsGranulocyte Colony-Stimulating FactorImmunity, InnateInterleukin-6Klebsiella InfectionsKlebsiella pneumoniaeMiceNeutrophilsPneumonia, BacterialSTAT3 Transcription FactorGranulocyte Colony-Stimulating FactorInterleukin-6Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID24470495
PMCPMC3944070
OpenAlexW2153711491

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.