Evidence map›Paper›PMID 18190610›Full record

ArticleClinical and experimental immunology2008

Neurotrophins modulate monocyte chemotaxis without affecting macrophage function.

B Samah, F Porcheray, G Gras

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Potential Neuroprotective Role of Neurotrophin in Traumatic Brain Injury.CNS & neurological disorders drug targets · 2024
    Review
  4. Article
  5. Review
  6. Neurotrophins: Neuroimmune Interactions in Human Atopic Diseases.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Role of NGF and its receptors in wound healing (Review).Experimental and therapeutic medicine · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. p75Glia · 2019
    Article
  17. Article
  18. Article
  19. NGF and Its Receptors in the Regulation of Inflammatory Response.International journal of molecular sciences · 2017
    Review
  20. Macrophage and nerve interaction in endometriosis.Journal of neuroinflammation · 2017
    Review
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

3 authors at 3 institutions in 1 country.

B SamahCEA, DSV, iMETI, SIV, UMR E-01 Université Paris Sud, IFR13 Institut Paris Sud Cytokines, Service d'Immuno-Virologie, Fontenay-aux Roses, France.
F Porcheray
G Gras
CEA Paris-Saclay - Etablissement de Fontenay-aux-roses · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurotrophins nerve growth factor (NGF), brain-derived growth factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4 (NT-4) and their high-affinity tyrosine protein kinase receptor (Trk) family, TrkA, TrkB, TrkC, and low-affinity p75(NTR) receptor, are key molecules implicated in the development of the central nervous system. Increasing evidence suggests that they also have physiological and pathological roles outside the nervous system. In this study we examined the expression of neurotrophins and their receptors in human activated macrophages and to what extent neurotrophins themselves modulate macrophage activation, in a model of primary adult monocyte-derived macrophage. Our data indicate that macrophages express neurotrophin and neurotrophin receptor genes differentially, and respond to cell stimulation by specific inductions. Neurotrophins did not modify the antigen-presenting capacities of macrophages or their production of proinflammatory cytokines, but somehow skewed their activation phenotype. In contrast, NGF clearly increased CXCR-4 expression in macrophage and their chemotactic response to low CXCL-12 concentration. The differential effect of specific macrophage stimuli on neurotrophin expression, in particular NGF and NT-3, and the specific enhancement of CXCR-4 expression suggest that neurotrophins might participate in tissue-healing mechanisms that should be investigated further in vivo.

Indexed as

Cell DifferentiationCells, CulturedChemokine CXCL12Chemotaxis, LeukocyteHumansImmunophenotypingLymphocyte Culture Test, MixedMacrophage ActivationMacrophagesMonocytesNerve Growth FactorNerve Growth FactorsReceptors, Nerve Growth FactorReverse Transcriptase Polymerase Chain ReactionChemokine CXCL12CXCL12 protein, humanNerve Growth FactorNerve Growth FactorsReceptors, Nerve Growth Factor

Identifiers

PMID18190610
PMCPMC2276974
OpenAlexW2169077424

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.