Evidence map›Paper›PMID 27928159›Full record

ArticleScientific reports2016

Effect of TREM-1 blockade and single nucleotide variants in experimental renal injury and kidney transplantation.

Alessandra Tammaro, Jesper Kers, Diba Emal, Ingrid Stroo, Gwendoline J D Teske, Loes M Butter, Nike Claessen, Jeffrey Damman, Marc Derive, Gerjan J Navis and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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, 34 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Alessandra TammaroDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Jesper KersDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Diba EmalDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Ingrid StrooDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Gwendoline J D TeskeDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Loes M ButterDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Nike ClaessenDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Jeffrey DammanDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Marc DeriveInserm UMR_S1116, Faculté de Médecine de Nancy, Université de Lorraine, Vandoeuvre-les-Nancy, France.
Gerjan J NavisDepartment of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Sandrine FlorquinDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Jaklien C LeemansDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Mark C DessingDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
University of Amsterdam · NLAcademic Medical Center · NLInserm · FRUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal ischemia reperfusion (IR)-injury induces activation of innate immune response which sustains renal injury and contributes to the development of delayed graft function (DGF). Triggering receptor expressed on myeloid cells-1 (TREM-1) is a pro-inflammatory evolutionary conserved pattern recognition receptor expressed on a variety of innate immune cells. TREM-1 expression increases following acute and chronic renal injury. However, the function of TREM-1 in renal IR is still unclear. Here, we investigated expression and function of TREM-1 in a murine model of renal IR using different TREM-1 inhibitors: LP17, LR12 and TREM-1 fusion protein. In a human study, we analyzed the association of non-synonymous single nucleotide variants in the TREM1 gene in a cohort comprising 1263 matching donors and recipients with post-transplant outcomes, including DGF. Our findings demonstrated that, following murine IR, renal TREM-1 expression increased due to the influx of Trem1 mRNA expressing cells detected by in situ hybridization. However, TREM-1 interventions by means of LP17, LR12 and TREM-1 fusion protein did not ameliorate IR-induced injury. In the human renal transplant cohort, donor and recipient TREM1 gene variant p.Thr25Ser was not associated with DGF, nor with biopsy-proven rejection or death-censored graft failure. We conclude that TREM-1 does not play a major role during experimental renal IR and after kidney transplantation.

Indexed as

AnimalsDelayed Graft FunctionGene Expression RegulationHumansInflammationKidneyKidney TransplantationLauric AcidsMiceOligopeptidesPolymorphism, Single NucleotideRecombinant Fusion ProteinsReperfusion InjuryRhodaminesTriggering Receptor Expressed on Myeloid Cells-1Lauric AcidsnangibotideOligopeptidesRecombinant Fusion ProteinsRhodaminesTriggering Receptor Expressed on Myeloid Cells-1

Identifiers

PMID27928159
PMCPMC5143803
OpenAlexW2560162242

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.