Evidence map›Paper›PMID 24872191›Full record

Trial reportJournal of immunology (Baltimore, Md. : 1950)2014

Podocytes regulate neutrophil recruitment by glomerular endothelial cells via IL-6-mediated crosstalk.

Sahithi J Kuravi, Helen M McGettrick, Simon C Satchell, Moin A Saleem, Lorraine Harper, Julie M Williams, George Ed Rainger, Caroline O S Savage

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Neutrophils and NETs in kidney disease.Nature reviews. Nephrology · 2025
    Review
  4. Review
  5. Article
  6. IL-6 and diabetic kidney disease.Frontiers in immunology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Emerging roles of infiltrating granulocytes and monocytes in homeostasis.Cellular and molecular life sciences : CMLS · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

Sahithi J KuraviCentre for Translational Inflammation Research, School of Immunity and Infection, University of Birmingham, Birmingham B15 2TT, United Kingdom; s.j.panchagnula@bham.ac.uk.
Helen M McGettrickSchool of Immunity and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom;
Simon C SatchellAcademic Renal Unit, Southmead Hospital, Bristol BS10 5NB, United Kingdom;
Moin A SaleemAcademic Renal Unit, Southmead Hospital, Bristol BS10 5NB, United Kingdom;
Lorraine HarperCentre for Translational Inflammation Research, School of Immunity and Infection, University of Birmingham, Birmingham B15 2TT, United Kingdom;
Julie M WilliamsWellcome Trust Clinical Research Facility, University Hospital Birmingham Foundation Trust, Birmingham B15 2TH, United Kingdom; and.
George Ed RaingerClinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom.
Caroline O S SavageSchool of Immunity and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom;
University of Birmingham · GBSouthmead Hospital · GBNIHR Wellcome Trust Southampton Clinical Research Facility · GB

Funding

Biotechnology and Biological Sciences Research Council BB/G000077/1Medical Research Council G0600069Medical Research Council RRAK 12708
6 · The paper itself

Abstract

Stromal cells actively modulate the inflammatory process, in part by influencing the ability of neighboring endothelial cells to support the recruitment of circulating leukocytes. We hypothesized that podocytes influence the ability of glomerular endothelial cells (GEnCs) to recruit neutrophils during inflammation. To address this, human podocytes and human GEnCs were cultured on opposite sides of porous inserts and then treated with or without increasing concentrations of TNF-α prior to addition of neutrophils. The presence of podocytes significantly reduced neutrophil recruitment to GEnCs by up to 50% when cultures were treated with high-dose TNF-α (100 U/ml), when compared with GEnC monocultures. Importantly, this phenomenon was dependent on paracrine actions of soluble IL-6, predominantly released by podocytes. A similar response was absent when HUVECs were cocultured with podocytes, indicating a tissue-specific phenomenon. Suppressor of cytokine signaling 3 elicited the immunosuppressive actions of IL-6 in a process that disrupted the presentation of chemokines on GEnCs by altering the expression of the duffy Ag receptor for chemokines. Interestingly, suppressor of cytokine signaling 3 knockdown in GEnCs upregulated duffy Ag receptor for chemokines and CXCL5 expression, thereby restoring the neutrophil recruitment. In summary, these studies reveal that podocytes can negatively regulate neutrophil recruitment to inflamed GEnCs by modulating IL-6 signaling, identifying a potential novel anti-inflammatory role of IL-6 in renal glomeruli.

Indexed as

Neutrophil InfiltrationCell CommunicationCell Line, TransformedEndothelial CellsFemaleGene Knockdown TechniquesHumansInterleukin-6MaleNeutrophilsPodocytesSOXB1 Transcription FactorsIL6 protein, humanInterleukin-6SOX3 protein, humanSOXB1 Transcription Factors

Identifiers

PMID24872191
PMCPMC4067868
OpenAlexW2098151682

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.