Evidence map›Paper›PMID 24342460›Full record

ArticleCritical care (London, England)2013

High-mobility group box 1 and the receptor for advanced glycation end products contribute to lung injury during Staphylococcus aureus pneumonia.

Ahmed Achouiti, Anne Jan van der Meer, Sandrine Florquin, Huan Yang, Kevin J Tracey, Cornelis van 't Veer, Alex F de Vos, Tom van der Poll

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  10. Article
  11. Review
  12. High-Mobility Group Box 1 (HMGB1) and Autophagy in Acute Lung Injury (ALI): A Review.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Review
  13. Article
  14. Article
  15. Sepsis and Pediatric Acute Respiratory Distress Syndrome.Journal of pediatric intensive care · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Ahmed Achouiti
Anne Jan van der Meer
Sandrine Florquin
Huan Yang
Kevin J Tracey
Cornelis van 't Veer
Alex F de Vos
Tom van der Poll
Academic Medical Center · NLUniversity of Amsterdam · NLFeinstein Institute for Medical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionStaphylococcus (S.) aureus has emerged as an important cause of necrotizing pneumonia. Lung injury during S. aureus pneumonia may be enhanced by local release of damage associated molecular patterns such as high-mobility group box 1 (HMGB1). In the current study we sought to determine the functional role of HMGB1 and its receptors, toll-like receptor 4 (TLR4) and the receptor for advanced glycation end products (RAGE), in the injurious host response to S. aureus pneumonia.

methodsPneumonia was induced in wild type (Wt), TLR4 deficient (tlr4-/-) and RAGE deficient (rage-/-) mice by intranasal inoculation of 1 × 107 colony-forming units (CFU) of a USA300 S. aureus. In a separate set of experiments, Wt mice were injected intraperitoneally with a monoclonal anti-HMGB1 antibody or an isotype matched control antibody immediately before and every 24 hours after intranasal infection of S. aureus. Mice were sacrificed at 6, 24, 48 or 72 hours after infection for harvesting of blood and organs.

resultsS. aureus pneumonia was associated with HMGB1 release in the bronchoalveolar compartment peaking after 24 hours. Anti-HMGB1 attenuated lung pathology and protein leak and reduced interleukin-1β release 6 hours after infection, but not at later time points. RAGE deficiency more modestly attenuated lung pathology without influencing protein leak, while TLR4 deficiency did not impact on lung injury.

conclusionThese data suggest that HMGB1 and RAGE, but not TLR4, contribute to lung injury accompanying the early phase of S. aureus pneumonia.

Indexed as

AnimalsBronchoalveolar Lavage FluidChemokinesCytokinesDisease Models, AnimalGlycation End Products, AdvancedHMGB1 ProteinLungMiceNeutrophilsPneumonia, StaphylococcalReceptor for Advanced Glycation End ProductsReceptors, ImmunologicToll-Like Receptor 4ChemokinesCytokinesGlycation End Products, AdvancedHMGB1 ProteinReceptor for Advanced Glycation End ProductsReceptors, ImmunologicToll-Like Receptor 4

Identifiers

PMID24342460
PMCPMC4057161
OpenAlexW2016389325

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.