Evidence map›Paper›PMID 20136829›Full record

ArticleBritish journal of pharmacology2010

The role of adenosine receptors in regulating production of tumour necrosis factor-alpha and chemokines by human lung macrophages.

A Buenestado, S Grassin Delyle, I Arnould, F Besnard, E Naline, S Blouquit-Laye, A Chapelier, J F Bellamy, P Devillier

Abstract read
In one paragraph

Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Dual blockade of adenosine AFrontiers in immunology · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. From Inflammation to the Onset of Fibrosis through AInternational journal of molecular sciences · 2020
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Purinergic signalling and immune cells.Purinergic signalling · 2014
    Review
  18. Article
  19. Article
  20. Regulation of macrophage function by adenosine.Arteriosclerosis, thrombosis, and vascular biology · 2012
    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

9 authors.

A BuenestadoLaboratory of Pulmonary Pharmacology UPRES EA220, Suresnes, France.
S Grassin Delyle
I Arnould
F Besnard
E Naline
S Blouquit-Laye
A Chapelier
J F Bellamy
P Devillier

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAdenosine is a major endogenous regulator of macrophage function, and activates four specific adenosine receptors (A(1), A(2A), A(2B) and A(3)). Here, we have assessed in human lung macrophages the modulation of the expression of adenosine receptor mRNA by lipopolysaccharide (LPS), and the relative contributions of the different adenosine receptors to LPS-induced production of tumour necrosis factor (TNF)-alpha and chemokines. EXPERIMENTAL APPROACH: Lung macrophages isolated from resected lungs were stimulated with LPS and treated with adenosine receptor agonists or/and antagonists. Adenosine receptor expression was assessed with qRT-PCR. Cytokines were measured in lung macrophage supernatants with elisa. KEY

resultsLPS increased (about 400-fold) mRNA for A(2A) adenosine receptors, decreased mRNA for A(1) and A(2B), but had no effect on A(3) adenosine receptor mRNA. The adenosine receptor agonist NECA inhibited TNF-alpha production concentration dependently, whereas the A(1) receptor agonist, CCPA, and the A(3) receptor agonist, AB-MECA, inhibited TNF-alpha production only at concentrations affecting A(2A) receptors. NECA also inhibited the production of CCL chemokines (CCL2, CCL3, CCL4, CCL5) and CXCL chemokines (CXCL9 and CXCL10), but not that of CXCL1, CXCL8 and CXCL5. Reversal of NECA-induced inhibition of TNF-alpha and chemokine production by the selective A(2A) adenosine receptor antagonist ZM 241385, but not the A(2B) receptor antagonist, MRS 1754, or the A(3) receptor antagonist, MRS 1220, indicated involvement of A(2A) receptors. CONCLUSIONS AND IMPLICATIONS: LPS up-regulated A(2A) adenosine receptor gene transcription, and this receptor subtype mediated inhibition of the LPS-induced production of TNF-alpha and of a subset of chemokines in human lung macrophages.

Indexed as

AcetamidesCells, CulturedChemokinesFemaleHumansLipopolysaccharidesLungMacrophages, AlveolarMaleMiddle AgedProtein SubunitsPurinergic P1 Receptor AgonistsPurinergic P1 Receptor AntagonistsPurinesQuinazolinesReceptors, Purinergic P19-chloro-2-(2-furyl)-5-phenylacetylamino(1,2,4)triazolo(1,5-c)quinazolineAcetamidesChemokineslipopolysaccharide, Escherichia coli O111 B4LipopolysaccharidesN-(4-cyanophenyl)-2-(4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-yl)-phenoxy)acetamideProtein SubunitsPurinergic P1 Receptor AgonistsPurinergic P1 Receptor AntagonistsPurinesQuinazolinesReceptors, Purinergic P1TriazinesTriazolesTumor Necrosis Factor-alphaZM 241385

Identifiers

PMID20136829
PMCPMC2848934

What OpenQuestion holds

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Registered trials

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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.