Evidence map›Paper›PMID 35053354›Full record

ArticleCells2022

S100A8/A9 Is a Marker for the Release of Neutrophil Extracellular Traps and Induces Neutrophil Activation.

Evelien G G Sprenkeler, Judith Zandstra, Nadine D van Kleef, Ines Goetschalckx, Bibian Verstegen, Cathelijn E M Aarts, Hans Janssen, Anton T J Tool, Gerard van Mierlo, Robin van Bruggen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
15.3field-weighted citation impact, top 1% 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

137 citing papers in PubMed, 194 citations in OpenAlex.

  1. Trial
  2. Efficacy and Safety of Recombinant Human Thrombopoietin (rhTPO) on Coagulation Function and Inflammatory Factors in the Treatment of Patients with Sepsis-Related Thrombocytopenia.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
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  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Galectin-9Aging cell · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Host immune dysfunction and Mycoplasma pneumoniae immune evasion: dual drivers of pathogenesis in Mycoplasma pneumoniae pneumonia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review

77 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

Evelien G G SprenkelerSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.ORCID 0000-0002-4961-0155
Judith ZandstraDepartment of Pediatric Immunology, Rheumatology and Infectious Diseases, Emma Children's Hospital, AUMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Nadine D van KleefSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.ORCID 0000-0001-7162-9277
Ines GoetschalckxSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Bibian VerstegenSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Cathelijn E M AartsSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Hans JanssenDivision of Biochemistry, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
Anton T J ToolSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Gerard van MierloSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Immunopathology, AUMC, University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Robin van BruggenSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Ilse JongeriusDepartment of Pediatric Immunology, Rheumatology and Infectious Diseases, Emma Children's Hospital, AUMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.ORCID 0000-0002-7759-9897
Taco W KuijpersSanquin Research and Laboratory Services and Landsteiner Laboratory, Department of Molecular Hematology, Amsterdam University Medical Center (AUMC), University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Sanquin · NLThe Netherlands Cancer Institute · NL

Funding

European Union's Horizon 2020 research and innovation programme 668303
6 · The paper itself

Abstract

Neutrophils are the most abundant innate immune cells in the circulation and they are the first cells recruited to sites of infection or inflammation. Almost half of the intracellular protein content in neutrophils consists of S100A8 and S100A9, though there has been controversy about their actual localization. Once released extracellularly, these proteins are thought to act as damage-associated molecular patterns (DAMPs), though their mechanism of action is not well understood. These S100 proteins mainly form heterodimers (S100A8/A9, also known as calprotectin) and this heterocomplex is recognized as a useful biomarker for several inflammatory diseases. We observed that S100A8/A9 is highly present in the cytoplasmic fraction of neutrophils and is not part of the granule content. Furthermore, we found that S100A8/A9 was not released in parallel with granular content but upon the formation of neutrophil extracellular traps (NETs). Accordingly, neutrophils of patients with chronic granulomatous disease, who are deficient in phorbol 12-myristate 13-acetate (PMA)-induced NETosis, did not release S100A8/A9 upon PMA stimulation. Moreover, we purified S100A8/A9 from the cytoplasmic fraction of neutrophils and found that S100A8/A9 could induce neutrophil activation, including adhesion and CD11b upregulation, indicating that this DAMP might amplify neutrophil activation.

Indexed as

Neutrophil ActivationCalgranulin ACalgranulin BCell DegranulationCytoplasmExocytosisExtracellular TrapsHumansNeutrophilsCalgranulin ACalgranulin BcalprotectinMRP8/14neutrophil extracellular trapsneutrophilsS100A8/A9

Identifiers

PMID35053354
PMCPMC8773660
OpenAlexW4205996427

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.