Evidence map›Paper›PMID 19737241›Full record

ArticleClinical and experimental immunology2009

Spatiotemporal expression of chemokines and chemokine receptors in experimental anti-myeloperoxidase antibody-mediated glomerulonephritis.

B S van der Veen, A H Petersen, J A Belperio, S C Satchell, P W Mathieson, G Molema, P Heeringa

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. CX3CL1-induced CD16Frontiers in immunology · 2022
    Article
  3. Observational
  4. Article
  5. Article
  6. CXCL5 drives neutrophil recruitment in TH17-mediated GN.Journal of the American Society of Nephrology : JASN · 2015
    Article
  7. Article
  8. Review
  9. Article
  10. Article
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

7 authors at 5 institutions in 3 countries.

B S van der VeenDepartment of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
A H Petersen
J A Belperio
S C Satchell
P W Mathieson
G Molema
P Heeringa
University Medical Center Groningen · NLSouthmead Hospital · GBUniversity of Bristol · GBUniversity of California, Los Angeles · USUniversity of Groningen · NL

Funding

Medical Research Council G0800200
6 · The paper itself

Abstract

Myeloperoxidase (MPO)-anti-neutrophil cytoplasmic autoantibody (ANCA)-associated necrotizing crescentic glomerulonephritis (NCGN) is characterized by abundant leucocyte infiltration. Chemokines are chemotactic cytokines involved in receptor-mediated recruitment of leucocytes. Our objective was to analyse spatiotemporal gene expression of chemokines and chemokine receptors in anti-MPO-mediated NCGN, to find potential targets for intervening with leucocyte influx. NCGN was induced in mice by co-administration of anti-MPO immunoglobulin (Ig)G and lipopolysaccharide. mRNA expression levels of chemokines and chemokine receptors were analysed in whole kidney lysates as well as in laser microdissected glomeruli and tubulo-interstitial tissue 1 and 7 day(s) after NCGN induction. Several chemokines and chemokine receptors were induced or up-regulated in anti-MPO-mediated NCGN, both on day 1 (chemokines CCL3, 5; CXCL2, 5, 13; receptor CXCR2) and on day 7 (chemokines CCL2, 5, 7, 8, 17, 20; CXCL1, 2, 5, 10; CX(3)CL1; receptors CCR2, 8; CX(3)CR1). The expression levels of most chemokines and receptors were higher in glomeruli than in the tubulo-interstitium. Because of the temporal induction of CXCR2 on day 1, we hypothesized CXCR2 as a potential target for treatment in anti-MPO-induced NCGN. Inhibition of CXCR2 using a goat-anti-CXCR2 serum prior to NCGN induction increased glomerular neutrophil influx but did not affect crescent formation and albuminuria. In conclusion, expression levels of various chemokines and chemokine receptors were increased in anti-MPO NCGN, and expressed particularly in glomeruli. These chemokines and receptors may serve as potential targets for treatment. Inhibition of a single target, CXCR2, did not attenuate anti-MPO NCGN. Combinatorial interventions may be necessary to avoid redundancy.

Indexed as

Gene Expression RegulationAnimalsAntibodies, Antineutrophil CytoplasmicChemokine CXCL1Chemokine CXCL2Chemokine CXCL5ChemokinesEndothelial CellsFemaleGene ExpressionGlomerulonephritisImmune SeraImmunoglobulin GKidney GlomerulusKidney TubulesLipopolysaccharidesAntibodies, Antineutrophil CytoplasmicChemokine CXCL1Chemokine CXCL2Chemokine CXCL5ChemokinesImmune SeraImmunoglobulin GLipopolysaccharidesPeroxidaseReceptors, ChemokineReceptors, Interleukin-8B

Identifiers

PMID19737241
PMCPMC2759069
OpenAlexW2129401109

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.