Evidence map›Paper›PMID 23087180›Full record

ArticleAnnals of the rheumatic diseases2013

Granulocyte colony stimulating factor exacerbates antineutrophil cytoplasmic antibody vasculitis.

Simon J Freeley, Alice M Coughlan, Reena J Popat, Deborah K Dunn-Walters, Michael G Robson

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Annals of the rheumatic diseases, 2013. 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Immunopathogenesis of ANCA-Associated Vasculitis.International journal of molecular sciences · 2020
    Review
  12. Coaxing Anti-Inflammatory Granulocytes to Prevent Ischemic Kidney Injury: A Fine Balance.Journal of the American Society of Nephrology : JASN · 2020
    Article
  13. Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020
    Review
  14. Article
  15. Re-Examining Neutrophil Participation in GN.Journal of the American Society of Nephrology : JASN · 2017
    Review
  16. Article
  17. An update on drug-induced arthritis.Rheumatology international · 2016
    Review
  18. Review
  19. Filgrastim-Induced Crescentic Transformation of Recurrent IgG2λ GN.Journal of the American Society of Nephrology : JASN · 2016
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Simon J FreeleyMedical Research Council (MRC) Centre for Transplantation, King's College London, London, UK.
Alice M Coughlan
Reena J Popat
Deborah K Dunn-Walters
Michael G Robson
King's College London · GB

Funding

Department of HealthMedical Research Council MR/J006742/1
6 · The paper itself

Abstract

objectivesGranulocyte colony stimulating factor (GCSF) is important in mobilising neutrophils from the bone marrow but also has a range of proinflammatory effects. We therefore decided to investigate the role of GCSF in antineutrophil cytoplasmic antibody (ANCA) vasculitis.

methodsWe measured GCSF levels in the serum of 38 patients with active ANCA vasculitis compared with 31 age-matched controls, and assessed the effect of GCSF priming on the response of human neutrophils to ANCA. We also examined the effect of exogenous GCSF administration in a murine model of antimyeloperoxidase (anti-MPO) vasculitis, and the effect of GCSF on murine neutrophil activation.

resultsThe serum levels of GCSF in patients with active ANCA vasculitis were significantly higher than those of age matched healthy controls (mean 38.04 vs 18.35 pg/ml, p<0.001). Furthermore, we demonstrated that GCSF primed human neutrophils in vitro for a respiratory burst in response to anti-MPO ANCA. In an anti-MPO antibody transfer model, mice given GCSF had more crescents (mean 29.1% vs 5.8% per glomerular cross section, p<0.05), more macrophages (mean 3.2 vs 1.2 per glomerular cross-section, p<0.01), higher serum creatines (mean 13.6 vs 8.3 μmol/l, p<0.05) and more haematuria (p<0.05) compared with controls. In vivo administration of GCSF with lipopolysaccharide (LPS), but not LPS alone, led to upregulation of CD11c on murine neutrophils.

conclusionsThese data suggest that GCSF, which is raised in patient serum, may play an important role in exacerbating disease in ANCA vasculitis. In addition, GCSF therapy for neutropenia should be used with caution in these patients.

Indexed as

AgedAnimalsAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisCase-Control StudiesDisease Models, AnimalDisease ProgressionFemaleGlomerulonephritisGranulocyte Colony-Stimulating FactorHumansMaleMiceNeutrophil ActivationNeutrophilsPeroxidaseGranulocyte Colony-Stimulating FactorPeroxidaseAutoantibodiesAutoimmune DiseasesInflammation

Identifiers

PMID23087180
OpenAlexW2109631994

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.