Evidence map›Paper›PMID 17875202›Full record

ArticleArthritis research & therapy2007

Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis.

Judith Auer, Markus Bläss, Hendrik Schulze-Koops, Stefan Russwurm, Thomas Nagel, Joachim R Kalden, Martin Röllinghoff, Horst Ulrich Beuscher

Open access · goldAbstract readComparative Study
In one paragraph

Article in Arthritis research & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 62 citations in OpenAlex.

  1. Serum PARC/CCL-18 concentrations and health outcomes in chronic obstructive pulmonary disease.American journal of respiratory and critical care medicine · 2011
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  2. Review
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  6. Article
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  12. Molecular Basis for CCRL2 Regulation of Leukocyte Migration.Frontiers in cell and developmental biology · 2020
    Review
  13. Review
  14. Evaluation of serum CCL18 as a potential biomarker for ovarian cancer.Cancer biomarkers : section A of Disease markers · 2017
    Article
  15. Re-Examining Neutrophil Participation in GN.Journal of the American Society of Nephrology : JASN · 2017
    Review
  16. Article
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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

8 authors at 3 institutions in 1 country.

Judith AuerInstitute for Clinical Microbiology, Immunology and Hygiene, University of Erlangen-Nuremberg, Wasserturmstrasse 3-5, D-91054 Erlangen, Germany. judithschlenk@hotmail.com
Markus Bläss
Hendrik Schulze-Koops
Stefan Russwurm
Thomas Nagel
Joachim R Kalden
Martin Röllinghoff
Horst Ulrich Beuscher
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEFriedrich Schiller University Jena · DEMolecular Networks (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is characterized by the recruitment of leukocytes and the accumulation of inflammatory mediators within the synovial compartment. Release of the chemokine CCL18 has been widely attributed to antigen-presenting cells, including macrophages and dendritic cells. This study investigates the production of CCL18 in polymorphonuclear neutrophils (PMN), the predominant cell type recruited into synovial fluid (SF). Microarray analysis, semiquantitative and quantitative reverse transcriptase polymerase chain reaction identified SF PMN from patients with RA as a novel source for CCL18 in diseased joints. Highly upregulated expression of other chemokine genes was observed for CCL3, CXCL8 and CXCL10, whereas CCL21 was downregulated. The chemokine receptor genes were differentially expressed, with upregulation of CXCR4, CCRL2 and CCR5 and downregulation of CXCR1 and CXCR2. In cell culture experiments, expression of CCL18 mRNA in blood PMN was induced by tumor necrosis factor alpha, whereas synthesis of CCL18 protein required additional stimulation with a combination of IL-10 and vitamin D3. In comparison, recruited SF PMN from patients with RA were sensitized for CCL18 production, because IL-10 alone was sufficient to induce CCL18 release. These results suggest a release of the T cell-attracting CCL18 by PMN when recruited to diseased joints. However, its production is tightly regulated at the levels of mRNA expression and protein synthesis.

Indexed as

AdultAgedAged, 80 and overArthritis, RheumatoidCells, CulturedChemokines, CCFemaleGene Expression RegulationHumansMaleMiddle AgedNeutrophilsSynovial FluidCCL18 protein, humanChemokines, CC

Identifiers

PMID17875202
PMCPMC2212580
OpenAlexW2134965930

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.