Evidence map›Paper›PMID 21072499›Full record

ArticleIntensive care medicine2011

Long pentraxin PTX3 deficiency worsens LPS-induced acute lung injury.

Bing Han, Jack J Haitsma, Yu Zhang, Xiaohui Bai, Matthew Rubacha, Shaf Keshavjee, Haibo Zhang, Mingyao Liu

Abstract read
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In one paragraph

Article in Intensive care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

40 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Hyaluronan: An Architect and Integrator for Cancer and Neural Diseases.International journal of molecular sciences · 2025
    Review
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  8. Expression of pentraxin 3 in equine lungs and neutrophils.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Hyaluronan interactions with innate immunity in lung biology.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
  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

8 authors at 3 institutions in 1 country.

Bing HanLatner Thoracic Surgery Research Laboratories, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Jack J Haitsma
Yu Zhang
Xiaohui Bai
Matthew Rubacha
Shaf Keshavjee
Haibo Zhang
Mingyao Liu
University Health Network · CASt. Michael's Hospital · CAUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research MOP-13270Canadian Institutes of Health Research MOP-42546
6 · The paper itself

Abstract

objectiveLong pentraxin PTX3 is an inflammatory mediator and a component of the humoral arm of innate immunity. PTX3 expression is increased in animals with acute lung injury (ALI) and in patients with sepsis or acute respiratory distress syndrome and is considered to be a potential biomarker for these diseases. However, the role of PTX3 in the pathogenesis of ALI is not fully understood. We hypothesized that PTX3, as an important immune modulator, may determine the severity of ALI.

methodsLipopolysaccharide (LPS) was intra-tracheally administrated to PTX3 knock-out (PTX3-KO) and wild-type (WT) mice. Lung injury, neutrophil infiltration, cell death, fibrin deposition, and tissue factor expression in the lung were determined. Local and systemic inflammatory responses were assessed by measuring cytokines in the lung and plasma.

resultsLPS instillation induced ALI in both PTX3-KO and WT mice. Interestingly, PTX3 deficiency significantly increased the magnitude/extent of lung injury compared to that in WT mice. The severe lung injury was accompanied by elevated neutrophil infiltration, cell death, and fibrin deposition in the lung. PTX3 deficiency also enhanced LPS-induced tissue factor expression/activation in the lung and increased tumor necrosis factor-alpha and monocyte chemoattractant protein-1 levels in the plasma.

conclusionOur data suggest that the endogenously expressed PTX3 plays a protective role in the pathogenesis of ALI and that a lack of PTX3 may enhance neutrophil recruitment, cell death, activation of coagulation cascades, and inflammatory responses in the lung.

Indexed as

Acute Lung InjuryAnimalsAnimals, Genetically ModifiedBlood CoagulationCell DeathC-Reactive ProteinGene Knockout TechniquesInflammationLipopolysaccharidesMiceNeutrophil InfiltrationPentraxinsSerum Amyloid P-ComponentSeverity of Illness IndexC-Reactive ProteinLipopolysaccharidesPentraxinsSerum Amyloid P-Component

Identifiers

PMID21072499
OpenAlexW2028239555

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.