Evidence map›Paper›PMID 26024383›Full record

Trial reportPloS one2015

Peptide 19-2.5 inhibits heparan sulfate-triggered inflammation in murine cardiomyocytes stimulated with human sepsis serum.

Lukas Martin, Susanne Schmitz, Rebecca De Santis, Sabine Doemming, Hajo Haase, Janine Hoeger, Lena Heinbockel, Klaus Brandenburg, Gernot Marx, Tobias Schuerholz

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2015. 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
2.1field-weighted citation impact, top 14% 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, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Pathogenesis and Treatment of Cytokine Storm Induced by Infectious Diseases.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Heparanase-enhanced Shedding of Syndecan-1 and Its Role in Driving Disease Pathogenesis and Progression.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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

10 authors at 4 institutions in 1 country.

Lukas MartinDepartment of Intensive Care and Intermediate Care, University Hospital, Aachen, Germany.
Susanne SchmitzDepartment of Intensive Care and Intermediate Care, University Hospital, Aachen, Germany.
Rebecca De SantisDepartment of Intensive Care and Intermediate Care, University Hospital, Aachen, Germany.
Sabine DoemmingDepartment of Intensive Care and Intermediate Care, University Hospital, Aachen, Germany.
Hajo HaaseDepartment of Food Chemistry and Toxicology, Berlin Institute of Technology, Berlin, Germany.
Janine HoegerInstitute of Immunology, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Lena HeinbockelDivision of Biophysics, Forschungszentrum, Borstel, Germany.
Klaus BrandenburgDivision of Biophysics, Forschungszentrum, Borstel, Germany.
Gernot MarxDepartment of Intensive Care and Intermediate Care, University Hospital, Aachen, Germany.
Tobias SchuerholzDepartment of Intensive Care and Intermediate Care, University Hospital, Aachen, Germany.
Universitätsklinikum Aachen · DEResearch Center Borstel - Leibniz Lung Center · DEFraunhofer Institute for Production Systems and Design Technology · DERWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial dysfunction in sepsis has been linked to inflammation caused by pathogen-associated molecular patterns (PAMPs) as well as by host danger-associated molecular patterns (DAMPs). These include soluble heparan sulfate (HS), which triggers the devastating consequences of the pro-inflammatory cascades in severe sepsis and septic shock. Thus, there is increasing interest in the development of anti-infective agents, with effectiveness against both PAMPs and DAMPs. We hypothesized that a synthetic antimicrobial peptide (peptide 19-2.5) inhibits inflammatory response in murine cardiomyocytes (HL-1 cells) stimulated with PAMPs, DAMPs or serum from patients with septic shock by reduction and/or neutralization of soluble HS. In the current study, our data indicate that the treatment with peptide 19-2.5 decreases the inflammatory response in HL-1 cells stimulated with either PAMPs or DAMPs. Furthermore, our work shows that soluble HS in serum from patients with Gram-negative or Gram-positive septic shock induces a strong pro-inflammatory response in HL-1 cells, which can be effectively blocked by peptide 19-2.5. Based on these findings, peptide 19-2.5 is a novel anti-inflammatory agent interacting with both PAMPs and DAMPs, suggesting peptide 19-2.5 may have the potential for further development as a broad-spectrum anti-inflammatory agent in sepsis-induced myocardial inflammation and dysfunction.

Indexed as

SerumAgedAnimalsAntimicrobial Cationic PeptidesCell LineFemaleHeparan SulfateHumansInflammationMaleMiceMiddle AgedMyocytes, CardiacSepsisAntimicrobial Cationic PeptidesHeparan Sulfate

Identifiers

PMID26024383
PMCPMC4449035
OpenAlexW1534122225

What OpenQuestion holds

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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.