Evidence map›Paper›PMID 21768189›Full record

ArticleThorax2011

PAI-1 is an essential component of the pulmonary host response during Pseudomonas aeruginosa pneumonia in mice.

Arnaud Goolaerts, Mathieu Lafargue, Yuanlin Song, Byron Miyazawa, Mehrdad Arjomandi, Michel Carlès, Jérémie Roux, Marybeth Howard, Dale A Parks, Karen E Iles and 1 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Thorax, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

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  12. α-Tocopherol Attenuates the Severity ofAmerican journal of respiratory cell and molecular biology · 2020
    Article
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  14. Review
  15. Article
  16. Prostaglandin E receptor-4 receptor mediates endothelial barrier-enhancing and anti-inflammatory effects of oxidized phospholipids.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  17. Article
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  19. Neuronal Wiskott-Aldrich syndrome protein regulates TGF-β1-mediated lung vascular permeability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    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

11 authors at 3 institutions in 2 countries.

Arnaud GoolaertsDepartment of Anesthesiology, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, USA.
Mathieu Lafargue
Yuanlin Song
Byron Miyazawa
Mehrdad Arjomandi
Michel Carlès
Jérémie Roux
Marybeth Howard
Dale A Parks
Karen E Iles
Jean-François Pittet
University of California, San Francisco · USUniversity of Alabama at Birmingham · USUniversité Côte d'Azur · FR

Funding

Coagulation Abnormalities and Post-Traumatic Ventilator-Associated PneumoniaR01GM086416 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PITTET, JEAN-FRANCOIS · 2010 to 2013
$1.2M
Osteopontin in Oxidative Injury and Airway Remodeling in AsthmaK23HL083099 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ARJOMANDI, MEHRDAD · 2006 to 2010
$744k
NHLBI NIH HHS K23 HL083099NIGMS NIH HHS GM086416NIGMS NIH HHS R01 GM086416
6 · The paper itself

Abstract

rationaleElevated plasma and bronchoalveolar lavage fluid plasminogen activator inhibitor 1 (PAI-1) levels are associated with adverse clinical outcome in patients with pneumonia caused by Pseudomonas aeruginosa. However, whether PAI-1 plays a pathogenic role in the breakdown of the alveolar-capillary barrier caused by P aeruginosa is unknown.

objectivesThe role of PAI-1 in pulmonary host defence and survival during P aeruginosa pneumonia in mice was tested. The in vitro mechanisms by which P aeruginosa causes PAI-1 gene and protein expression in lung endothelial and epithelial cells were also examined. METHODS AND

resultsPAI-1 null and wild-type mice that were pretreated with the PAI-1 inhibitor Tiplaxtinin had a significantly lower increase in lung vascular permeability than wild-type littermates after the airspace instillation of 1×10(7) colony-forming units (CFU) of P aeruginosa bacteria. Furthermore, P aeruginosa in vitro induced the expression of the PAI-1 gene and protein in a TLR4/p38/RhoA/NF-κB (Toll-like receptor 4/p38/RhoA/nuclear factor-κB) manner in lung endothelial and alveolar epithelial cells. However, in vivo disruption of PAI-1 signalling was associated with higher mortality at 24 h (p<0.03) and higher bacterial burden in the lungs secondary to decreased neutrophil migration into the distal airspace in response to P aeruginosa.

conclusionsThe results indicate that PAI-1 is a critical mediator that controls the development of the early lung inflammation that is required for the activation of the later innate immune response necessary for the eradication of P aeruginosa from the distal airspaces of the lung.

Indexed as

Gene Expression RegulationAnimalsBiomarkersBlotting, WesternBronchoalveolar Lavage FluidCells, CulturedDisease Models, AnimalDNAEndothelial CellsHumansLungMiceMice, Inbred C57BLPlasminogen Activator Inhibitor 1Pneumonia, BacterialPseudomonas aeruginosaBiomarkersDNAPlasminogen Activator Inhibitor 1

Identifiers

PMID21768189
PMCPMC3282176
OpenAlexW2170783786

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.