Evidence map›Paper›PMID 18566440›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Acrolein inhalation suppresses lipopolysaccharide-induced inflammatory cytokine production but does not affect acute airways neutrophilia.

David Itiro Kasahara, Matthew E Poynter, Ziryan Othman, David Hemenway, Albert van der Vliet

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  5. Article
  6. Alda-1 Protects Against Acrolein-Induced Acute Lung Injury and Endothelial Barrier Dysfunction.American journal of respiratory cell and molecular biology · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Molecular mechanisms of acrolein toxicity: relevance to human disease.Toxicological sciences : an official journal of the Society of Toxicology · 2015
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Exposure to acrolein by inhalation causes platelet activation.Toxicology and applied pharmacology · 2010
    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 2 institutions in 1 country.

David Itiro KasaharaDepartment of Pathology, Vermont Lung Center, College of Medicine, University of Vermont, Burlington, VT 05405, USA.
Matthew E Poynter
Ziryan Othman
David Hemenway
Albert van der Vliet
University of Vermont · USLung Institute · US

Funding

Cigarette Smoke-derived Electrophilic Aldehydes and Airway InflammationR01ES021476 · NIEHS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2012 to 2016
$1.9M
NITRIC OXIDE SIGNALING IN ALLERGIC AIRWAY DISEASER01HL074295 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2004 to 2007
$1.5M
TOXIC ALDEHYDES AS MODULATORS OF LUNG INFLAMMATIONR01HL068865 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2003 to 2007
$1.5M
NHLBI NIH HHS HL074295NHLBI NIH HHS R01 HL068865NHLBI NIH HHS R01 HL074295NIEHS NIH HHS R01 ES021476
6 · The paper itself

Abstract

Acrolein is a reactive unsaturated aldehyde that is produced during endogenous oxidative processes and is a major bioactive component of environmental pollutants such as cigarette smoke. Because in vitro studies demonstrate that acrolein can inhibit neutrophil apoptosis, we evaluated the effects of in vivo acrolein exposure on acute lung inflammation induced by LPS. Male C57BL/6J mice received 300 microg/kg intratracheal LPS and were exposed to acrolein (5 parts per million, 6 h/day), either before or after LPS challenge. Exposure to acrolein either before or after LPS challenge did not significantly affect the overall extent of LPS-induced lung inflammation, or the duration of the inflammatory response, as observed from recovered lung lavage leukocytes and histology. However, exposure to acrolein after LPS instillation markedly diminished the LPS-induced production of several inflammatory cytokines, specifically TNF-alpha, IL-12, and the Th1 cytokine IFN-gamma, which was associated with reduction in NF-kappaB activation. Our data demonstrate that acrolein exposure suppresses LPS-induced Th1 cytokine responses without affecting acute neutrophilia. Disruption of cytokine signaling by acrolein may represent a mechanism by which smoking contributes to chronic disease in chronic obstructive pulmonary disease and asthma.

Indexed as

AcroleinAcute DiseaseAdministration, InhalationAnimalsApoptosisCytokinesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesLung DiseasesMaleMiceMice, Inbred C57BLNeutrophilsNF-kappa BTh1 CellsTh2 CellsAcroleinCytokinesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesNF-kappa B

Identifiers

PMID18566440
PMCPMC3031871
OpenAlexW2096491268

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.