Evidence map›Paper›PMID 21726210›Full record

ArticleBritish journal of pharmacology2012

Azithromycin distinctively modulates classical activation of human monocytes in vitro.

M Vrančić, M Banjanac, K Nujić, M Bosnar, T Murati, V Munić, D Stupin Polančec, D Belamarić, M J Parnham, V Eraković Haber

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. The efficacy and safety of azithromycin in asthma: A systematic review.Journal of cellular and molecular medicine · 2019
    Pooled it
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  8. Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
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3 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

M VrančićGlaxoSmithKline Research Centre Zagreb Limited, Zagreb, Croatia. mila.vrancic@glpg.com
M Banjanac
K Nujić
M Bosnar
T Murati
V Munić
D Stupin Polančec
D Belamarić
M J Parnham
V Eraković Haber
Galapagos (Croatia) · HRGlaxoSmithKline (Croatia) · HRUniversity of Zagreb · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAzithromycin has been reported to modify activation of macrophages towards the M2 phenotype. Here, we have sought to identify the mechanisms underlying this modulatory effect of azithromycin on human monocytes, classically activated in vitro. EXPERIMENTAL APPROACH: Human blood monocytes were primed with IFN-γ for 24 h and activated with LPS for 24 h. Azithromycin, anti-inflammatory and lysosome-affecting agents were added 2 h before IFN-γ. Cytokine and chemokine expression was determined by quantitative PCR and protein release by ELISA. Signalling molecules were determined by Western blotting and transcription factor activation quantified with a DNA-binding ELISA kit. KEY

resultsAzithromycin (1.5-50 µM) dose-dependently inhibited gene expression and/or release of M1 macrophage markers (CCR7, CXCL 11 and IL-12p70), but enhanced CCL2, without altering TNF-α or IL-6. Azithromycin also enhanced the gene expression and/or release of M2 macrophage markers (IL-10 and CCL18), and the pan-monocyte marker CD163, but inhibited that of CCL22. The Toll-like receptor (TLR) 4 signalling pathway was modulated, down-regulating NF-κB and STAT1 transcription factors. The inhibitory profile of azithromycin differed from that of dexamethasone, the phosphodiesterase-4 inhibitor roflumilast and the p38 kinase inhibitor SB203580 but was similar to that of the lysosomotropic drug chloroquine. Effects of concanamycin and NH4Cl, which also act on lysosomes, differed significantly. CONCLUSIONS AND IMPLICATIONS: Azithromycin modulated classical activation of human monocytes by inhibition of TLR4-mediated signalling and possible effects on lysosomal function, and generated a mediator expression profile that differs from that of monocyte/macrophage phenotypes so far described.

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticAnti-Inflammatory AgentsAzithromycinCD163 AntigenCells, CulturedChemokine CCL2Chemokine CCL22Chemokines, CCDown-RegulationGene ExpressionHumansInterferon-gammaInterleukin-10Interleukin-6LipopolysaccharidesAntigens, CDAntigens, Differentiation, MyelomonocyticAnti-Inflammatory AgentsAzithromycinCCL18 protein, humanCCL22 protein, humanCCL2 protein, humanCD163 AntigenChemokine CCL2Chemokine CCL22Chemokines, CCIL10 protein, humanIL6 protein, humanInterferon-gammaInterleukin-10Interleukin-6LipopolysaccharidesNF-kappa BReceptors, Cell SurfaceSTAT1 protein, humanSTAT1 Transcription FactorTLR4 protein, humanToll-Like Receptor 4Transcription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID21726210
PMCPMC3372721
OpenAlexW1568457937

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.