Evidence map›Paper›PMID 23042197›Full record

ArticleShock (Augusta, Ga.)2012

STAT3-mediated IL-17 production by postseptic T cells exacerbates viral immunopathology of the lung.

Sumanta Mukherjee, Ronald M Allen, Nicholas W Lukacs, Steven L Kunkel, William F Carson

Open access · greenAbstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Supplementation with GPR120 (Ffar4) ligand omega-3 does not improve survival in murine sepsis models.American journal of physiology. Endocrinology and metabolism · 2025
    Article
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  4. Review
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  10. Observational
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  12. Article
  13. Article
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  15. Article
  16. Resistant pathogens, fungi, and viruses.The Surgical clinics of North America · 2014
    Review
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  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Sumanta MukherjeeDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
Ronald M Allen
Nicholas W Lukacs
Steven L Kunkel
William F Carson
University of Michigan–Ann Arbor · US

Funding

MONOKINE GENE EXPRESSION/REGULATION IN LUNG INJURYR01HL031237 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KUNKEL, STEVEN LYNN, STANDIFORD, THEODORE J. · 1985 to 2017
$5.9M
TLR and Notch Ligand in RSV-induced DiseaseR01AI073876 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 2008 to 2012
$1.9M
NHLBI NIH HHS R01 HL031237NHLBI NIH HHS R01HL031237-27NIAID NIH HHS R01 AI073876NIAID NIH HHS R01AI073876-03
6 · The paper itself

Abstract

Survivors of severe sepsis exhibit increased morbidity and mortality in response to secondary infections. Although bacterial secondary infections have been widely studied, there remains a paucity of data concerning viral infections after sepsis. In an experimental mouse model of severe sepsis (cecal ligation and puncture [CLP]) followed by respiratory syncytial virus (RSV) infection, exacerbated immunopathology was observed in the lungs of CLP mice compared with RSV-infected sham surgery mice. This virus-associated immunopathology was evidenced by increased mucus production in the lungs of RSV-infected CLP mice and correlated with increased IL-17 production in the lungs. Respiratory syncytial virus-infected CLP mice exhibited increased levels of TH2 cytokines and reduced interferon γ in the lungs and lymph nodes compared with RSV-infected sham mice. In addition, CD4 T cells from CLP mice produced increased IL-17 in vitro irrespective of the presence of exogenous cytokines or blocking antibodies. This increased IL-17 production correlated with increased STAT3 transcription factor binding to the IL-17 promoter in CD4 T cells from CLP mice. Furthermore, in vivo neutralization of IL-17 before RSV infection led to a significant reduction in virus-induced mucus production and TH2 cytokines. Taken together, these data provide evidence that postseptic CD4 T cells are primed toward IL-17 production via increased STAT3-mediated gene transcription, which may contribute to the immunopathology of a secondary viral infection.

Indexed as

Respiratory Syncytial VirusesAnimalsDisease Models, AnimalFemaleGene Expression RegulationInterferon-gammaInterleukin-17LungMiceMice, Inbred BALB CRespiratory Syncytial Virus InfectionsSepsisSTAT3 Transcription FactorTh2 CellsInterferon-gammaInterleukin-17Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID23042197
PMCPMC3475732
OpenAlexW2010786042

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.