Evidence map›Paper›PMID 18192501›Full record

ArticleAmerican journal of respiratory cell and molecular biology2008

Alveolar epithelial STAT3, IL-6 family cytokines, and host defense during Escherichia coli pneumonia.

Lee J Quinton, Matthew R Jones, Bryanne E Robson, Benjamin T Simms, Jeffrey A Whitsett, Joseph P Mizgerd

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

83 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
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  12. Article
  13. Article
  14. Epithelial STAT3: A New Twist in Inducible Antimicrobial Resistance.American journal of respiratory cell and molecular biology · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Epithelial LIF signaling limits apoptosis and lung injury during bacterial pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  19. Article
  20. Article

23 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

6 authors at 2 institutions in 2 countries.

Lee J QuintonMolecular and Integrative Physiological Sciences Program, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115, USA.
Matthew R Jones
Bryanne E Robson
Benjamin T Simms
Jeffrey A Whitsett
Joseph P Mizgerd
Department of Physiological Sciences · RUCincinnati Children's Hospital Medical Center · US

Funding

Translational Research Support CoreP30ES000002 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI SUSAN A KORRICK · 1985 to 2026
$44.6M
Training Program in Molecular and Integrative Physiological SciencesT32HL007118 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI LU, QUAN · 1985 to 2025
$14.3M
NF-KB and Innate Immunity in the LungsR01HL068153 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI MIZGERD, JOSEPH P · 2003 to 2016
$5.1M
Regulation and function of STAT3 during pneumoniaR01HL079392 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI MIZGERD, JOSEPH P · 2005 to 2015
$4.0M
NHLBI NIH HHS HL07118NHLBI NIH HHS HL079392NHLBI NIH HHS HL68153NIEHS NIH HHS ES00002
6 · The paper itself

Abstract

While signal transducer and activator of transcription (STAT) 3 signaling has been linked to multiple pathways influencing immune function and cell survival, the direct influence of this transcription factor on innate immunity and tissue homeostasis during pneumonia is unknown. Human patients with dominant-negative mutations in the Stat3 gene develop recurrent pneumonias, suggesting a role for STAT3 in pulmonary host defense. We hypothesized that alveolar epithelial STAT3 is activated by IL-6 family cytokines and is required for effective responses during gram-negative bacterial pneumonia. STAT3 phosphorylation was increased in pneumonic mouse lungs and in murine lung epithelial (MLE)-15 cells stimulated with pneumonic bronchoalveolar lavage fluid (BALF) through 48 hours of Escherichia coli pneumonia. Mice lacking active STAT3 in alveolar epithelial cells (Stat3(Delta/Delta)) had fewer alveolar neutrophils and more viable bacteria than control mice early after intratracheal E. coli. By 48 hours after E. coli infection, however, lung injury was increased in Stat3(Delta/Delta) mice. Bacteria were cleared from lungs of both genotypes, albeit more slowly in Stat3(Delta/Delta) mice. Of the IL-6 family cytokines measured in lungs from infected C57BL/6 mice, IL-6, oncostatin M, leukemia inhibitory factor (LIF), and IL-11 were significantly elevated. Neutralization studies demonstrated that LIF and IL-6 mediated BALF-induced STAT3 activation in MLE-15 cells. Together, these results indicate that during E. coli pneumonia, select IL-6 family members activate alveolar epithelial STAT3, which functions to promote neutrophil recruitment and to limit both infection and lung injury.

Indexed as

LungPulmonary AlveoliAnimalsCell LineChemokinesCytokinesEpithelial CellsEscherichia coli InfectionsHumansInflammationInterleukin-6MiceMice, Inbred C57BLMice, TransgenicPneumonia, BacterialSTAT3 Transcription FactorChemokinesCytokinesInterleukin-6STAT3 Transcription FactorVascular Endothelial Growth Factor A

Identifiers

PMID18192501
PMCPMC2396249
OpenAlexW2114249751

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.