Evidence map›Paper›PMID 31756204›Full record

ArticlePloS one2019

Mitochondrial alarmins are tissue mediators of ventilator-induced lung injury and ARDS.

Serge Grazioli, Irène Dunn-Siegrist, Laure-Anne Pauchard, Mathieu Blot, Pierre-Emmanuel Charles, Jérôme Pugin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.3field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Role of Dual Oxidases in Ventilator-induced Lung Injury.American journal of respiratory cell and molecular biology · 2021
    Article
  15. Review
  16. Observational
  17. Mitochondrial dysfunction in lung ageing and disease.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  18. PEBP1 acts as a rheostat between prosurvival autophagy and ferroptotic death in asthmatic epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

6 authors at 3 institutions in 2 countries.

Serge GrazioliIntensive Care Laboratory, Department of Microbiology and Molecular Medicine, University Hospitals of Geneva & Faculty of Medicine, Genève, Switzerland.ORCID 0000-0002-5526-851X
Irène Dunn-SiegristIntensive Care Laboratory, Department of Microbiology and Molecular Medicine, University Hospitals of Geneva & Faculty of Medicine, Genève, Switzerland.
Laure-Anne PauchardIntensive Care Unit, University Hospital of Dijon, Dijon, France.
Mathieu BlotDepartment of Infectious Diseases, University Hospital of Dijon, Dijon, France.
Pierre-Emmanuel CharlesIntensive Care Unit, University Hospital of Dijon, Dijon, France.
Jérôme PuginIntensive Care Laboratory, Department of Microbiology and Molecular Medicine, University Hospitals of Geneva & Faculty of Medicine, Genève, Switzerland.
Université de Bourgogne · FRMaison des Sciences sociales et des Humanités de Dijon · FRUniversity Hospital of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleEndogenous tissue mediators inducing lung inflammation in the context of ventilator-induced lung injury (VILI) and acute respiratory distress syndrome (ARDS) are ill-defined.

objectivesTo test whether mitochondrial alarmins are released during VILI, and are associated with lung inflammation.

methodsRelease of mitochondrial DNA, adenosine triphosphate (ATP), and formyl-Met-Leu-Phe (fMLP) peptide-dependent neutrophil chemotaxis were measured in conditioned supernatants from human alveolar type II-like (A549) epithelial cells submitted to cyclic stretch in vitro. Similar measurements were performed in bronchoalveolar lavage fluids from rabbits submitted to an injurious ventilatory regimen, and from patients with ARDS. MEASUREMENTS AND MAIN

resultsMitochondrial DNA was released by A549 cells during cell stretching, and was found elevated in BAL fluids from rabbits during VILI, and from ARDS patients. Cyclic stretch-induced interleukin-8 (IL-8) of A549 cells could be inhibited by Toll-like receptor 9 (TLR9) blockade. ATP concentrations were increased in conditioned supernatants from A549 cells, and in rabbit BAL fluids during VILI. Neutrophil chemotaxis induced by A549 cells conditioned supernatants was essentially dependent on fMLP rather than IL-8. A synergy between cyclic stretch-induced alarmins and lipopolysaccharide (LPS) was found in monocyte-derived macrophages in the production of IL-1ß.

conclusionsMitochondrial alarmins are released during cyclic stretch of human epithelial cells, as well as in BAL fluids from rabbits ventilated with an injurious ventilatory regimen, and found in BAL fluids from ARDS patients, particularly in those with high alveolar inflammation. These alarmins are likely to represent the proximal endogenous mediators of VILI and ARDS, released by injured pulmonary cells.

Indexed as

A549 CellsAlarminsAnimalsBronchoalveolar Lavage FluidCulture Media, ConditionedDNA, MitochondrialHumansInterleukin-8MacrophagesMaleMitochondriaNeutrophil InfiltrationOligoribonucleotides, AntisenseRabbitsRespiratory Distress SyndromeStress, PhysiologicalAlarminsCulture Media, ConditionedDNA, MitochondrialInterleukin-8Oligoribonucleotides, AntisenseToll-Like Receptor 9

Identifiers

PMID31756204
PMCPMC6874419
OpenAlexW2990714662

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.