Evidence map›Paper›PMID 25214442›Full record

ArticleBlood2014

Monocytic cell differentiation from band-stage neutrophils under inflammatory conditions via MKK6 activation.

René Köffel, Anastasia Meshcheryakova, Joanna Warszawska, Annika Hennig, Karin Wagner, Almut Jörgl, Daniela Gubi, Doris Moser, Anastasiya Hladik, Ulrike Hoffmann and 7 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2014. 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Target neutrophil heterogeneity and plasticity in cancer.Journal of hematology & oncology · 2025
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  6. Macrophage HM13/SPP Enhances Foamy Macrophage Formation and Atherogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Liposomal Nanotraps NeutralizeInfectious microbes & diseases · 2025
    Article
  8. Review
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  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

17 authors at 5 institutions in 3 countries.

René KöffelInstitute of Immunology, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria; Institute of Pathophysiology and Immunology, Center of Molecular Medicine, Medical University Graz, Graz, Austria;
Anastasia MeshcheryakovaInstitute of Immunology, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria;
Joanna WarszawskaCenter of Excellence for Medical Multimedia (CeMM), Research Center for Molecular Medicine of the Austrian Academy of Sciences and Department of Internal Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria;
Annika HennigInstitute of Immunology, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria;
Karin WagnerCenter for Medical Research, Medical University Graz, Graz, Austria;
Almut JörglInstitute of Immunology, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria;
Daniela GubiInstitute of Immunology, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria;
Doris MoserDepartment of Craniofacial, Maxillofacial and Oral Surgery.
Anastasiya HladikDivision of Rheumatology, Medicine III, and.
Ulrike HoffmannInstitute of Pathophysiology and Immunology, Center of Molecular Medicine, Medical University Graz, Graz, Austria;
Michael B FischerDepartment of Blood Group Serology and Transfusion Medicine, Medical University of Vienna, Vienna, Austria; and.
Wim van den BergDepartment of Rheumatology, Rheumatology Research and Advanced Therapeutics, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Marije KoendersDepartment of Rheumatology, Rheumatology Research and Advanced Therapeutics, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Clemens ScheineckerDivision of Rheumatology, Medicine III, and.
Bernhard GesslbauerInstitute of Immunology, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria;
Sylvia KnappCenter of Excellence for Medical Multimedia (CeMM), Research Center for Molecular Medicine of the Austrian Academy of Sciences and Department of Internal Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria;
Herbert StroblInstitute of Immunology, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria; Institute of Pathophysiology and Immunology, Center of Molecular Medicine, Medical University Graz, Graz, Austria;
Medical University of Vienna · ATMedical University of Graz · ATCenter for Rheumatology · USRadboud University Nijmegen · NLAustrian Academy of Sciences · AT

Funding

Austrian Science Fund FWF P 23215
6 · The paper itself

Abstract

During inflammation, neutrophils are rapidly mobilized from the bone marrow storage pool into peripheral blood (PB) to enter lesional sites, where most rapidly undergo apoptosis. Monocytes constitute a second wave of inflammatory immigrates, giving rise to long-lived macrophages and dendritic cell subsets. According to descriptive immunophenotypic and cell culture studies, neutrophils may directly "transdifferentiate" into monocytes/macrophages. We provide mechanistic data in human and murine models supporting the existence of this cellular pathway. First, the inflammatory signal-induced MKK6-p38MAPK cascade activates a monocyte differentiation program in human granulocyte colony-stimulating factor-dependent neutrophils. Second, adoptively transferred neutrophils isolated from G-CSF-pretreated mice rapidly acquired monocyte characteristics in response to inflammatory signals in vivo. Consistently, inflammatory signals led to the recruitment of osteoclast progenitor cell potential from ex vivo-isolated G-CSF-mobilized human blood neutrophils. Monocytic cell differentiation potential was retained in left-shifted band-stage neutrophils but lost in neutrophils from steady-state PB. MKK6-p38MAPK signaling in HL60 model cells led to diminishment of the transcription factor C/EBPα, which enabled the induction of a monocytic cell differentiation program. Gene profiling confirmed lineage conversion from band-stage neutrophils to monocytic cells. Therefore, inflammatory signals relayed by the MKK6-p38MAPK cascade induce monocytic cell differentiation from band-stage neutrophils.

Indexed as

AnimalsBlotting, WesternCCAAT-Enhancer-Binding Protein-alphaCell DifferentiationCells, CulturedEnzyme ActivationFlow CytometryGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorHL-60 CellsHumansInflammationInterleukin-1betaMAP Kinase Kinase 6Mice, Inbred C57BLMonocytesCCAAT-Enhancer-Binding Protein-alphaGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-1betaMAP2K6 protein, humanMAP Kinase Kinase 6p38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alpha

Identifiers

PMID25214442
PMCPMC4536888
OpenAlexW1992337146

What OpenQuestion holds

Textmetadata
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.