Evidence map›Paper›PMID 15972949›Full record

ArticleThe American journal of pathology2005

Inhibition of macrophage nuclear factor-kappaB leads to a dominant anti-inflammatory phenotype that attenuates glomerular inflammation in vivo.

Heather M Wilson, Salah Chettibi, Christian Jobin, David Walbaum, Andrew J Rees, David C Kluth

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

35 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
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  7. Article
  8. Review
  9. The varying roles of macrophages in kidney injury and repair.Current opinion in nephrology and hypertension · 2020
    Review
  10. Macrophage Phenotype and Fibrosis in Diabetic Nephropathy.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Controlled release strategies for modulating immune responses to promote tissue regeneration.Journal of controlled release : official journal of the Controlled Release Society · 2015
    Review
  17. Dendritic Cells and Macrophages: Sentinels in the Kidney.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Review
  18. Macrophage Phenotype in Kidney Injury and Repair.Kidney diseases (Basel, Switzerland) · 2015
    Review
  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

6 authors at 4 institutions in 6 countries.

Heather M WilsonDepartment of Medicine and Therapeutics, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen, Scotland, AB25 2ZD, UK. h.m.wilson@abdn.ac.uk
Salah Chettibi
Christian Jobin
David Walbaum
Andrew J Rees
David C Kluth
General Electric (Spain) · ESUniversity of Aberdeen · GBUniversity of Bío-Bío · CLUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infiltrating macrophages (mphi) can cause injury or facilitate repair, depending on how they are activated by the microenvironment. Studies in vitro have defined the roles of individual cytokines and signaling pathways in activation, but little is known about how macrophages integrate the multiple signals they receive in vivo. We inhibited nuclear factor-kappaB in bone marrow-derived macrophages (BMDMs) by using a recombinant adenovirus expressing dominant-negative IkappaB (Ad-IkappaB). This re-orientated macrophage activation so they became profoundly anti-inflammatory in settings where they would normally be classically activated. In vitro, the lipopolysaccharide-induced nitric oxide, interleukin-12, and tumor necrosis factor-alpha synthesis was abrogated while interleukin-10 synthesis increased. In vivo, fluorescently labeled BMDMs transduced with Ad-IkappaB and injected into the renal artery significantly reduced inducible nitric oxide synthase and MHC class II expression when activated naturally in glomeruli of rats with nephrotoxic nephritis. Furthermore, although they only comprised 15% of glomerular macrophages, their presence significantly reduced glomerular infiltration and activation of host macrophages. Injury in nephrotoxic nephritis was also decreased when assessed morphologically and by severity of albuminuria. The results demonstrate the power of Ad-IkappaB-transduced BMDMs to inhibit injury when activated by acute immune-mediated inflammation within the glomerulus.

Indexed as

AnimalsBone Marrow CellsElectrophoretic Mobility Shift AssayFlow CytometryInflammationInterleukin-10In Vitro TechniquesKidney GlomerulusMacrophage ActivationMacrophagesNephritisNF-kappa BPhenotypeRatsTransduction, GeneticInterleukin-10NF-kappa B

Identifiers

PMID15972949
PMCPMC1603438
OpenAlexW2060979962

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.