Evidence map›Paper›PMID 17064416›Full record

ArticleRespiratory research2006

Azithromycin reduces spontaneous and induced inflammation in DeltaF508 cystic fibrosis mice.

Rachida Legssyer, François Huaux, Jean Lebacq, Monique Delos, Etienne Marbaix, Patrick Lebecque, Dominique Lison, Bob J Scholte, Pierre Wallemacq, Teresinha Leal

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Azithromycin through the Lens of the COVID-19 Treatment.Antibiotics (Basel, Switzerland) · 2022
    Review
  6. Review
  7. Azithromycin in viral infections.Reviews in medical virology · 2021
    Review
  8. Review
  9. Review
  10. Article
  11. CFTR Modulators DampenFrontiers in cellular and infection microbiology · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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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 2 institutions in 2 countries.

Rachida LegssyerClinical Chemistry, Université Catholique de Louvain, Ave Hippocrate 10, Brussels, Belgium. rlegssyer@yahoo.fr
François Huaux
Jean Lebacq
Monique Delos
Etienne Marbaix
Patrick Lebecque
Dominique Lison
Bob J Scholte
Pierre Wallemacq
Teresinha Leal
UCLouvain · BEErasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammation plays a critical role in lung disease development and progression in cystic fibrosis. Azithromycin is used for the treatment of cystic fibrosis lung disease, although its mechanisms of action are poorly understood. We tested the hypothesis that azithromycin modulates lung inflammation in cystic fibrosis mice.

methodsWe monitored cellular and molecular inflammatory markers in lungs of cystic fibrosis mutant mice homozygous for the DeltaF508 mutation and their littermate controls, either in baseline conditions or after induction of acute inflammation by intratracheal instillation of lipopolysaccharide from Pseudomonas aeruginosa, which would be independent of interactions of bacteria with epithelial cells. The effect of azithromycin pretreatment (10 mg/kg/day) given by oral administration for 4 weeks was evaluated.

resultsIn naive cystic fibrosis mice, a spontaneous lung inflammation was observed, characterized by macrophage and neutrophil infiltration, and increased intra-luminal content of the pro-inflammatory cytokine macrophage inflammatory protein-2. After induced inflammation, cystic fibrosis mice combined exaggerated cellular infiltration and lower anti-inflammatory interleukin-10 production. In cystic fibrosis mice, azithromycin attenuated cellular infiltration in both baseline and induced inflammatory condition, and inhibited cytokine (tumor necrosis factor-alpha and macrophage inflammatory protein-2) release in lipopolysaccharide-induced inflammation.

conclusionOur findings further support the concept that inflammatory responses are upregulated in cystic fibrosis. Azithromycin reduces some lung inflammation outcome measures in cystic fibrosis mice. We postulate that some of the benefits of azithromycin treatment in cystic fibrosis patients are due to modulation of lung inflammation.

Indexed as

AnimalsAnti-Inflammatory AgentsAzithromycinChemokine CXCL2Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorInterleukin-10LipopolysaccharidesLungMacrophagesMiceMice, Mutant StrainsMonokinesNeutrophil InfiltrationPneumoniaTumor Necrosis Factor-alphaAnti-Inflammatory AgentsAzithromycinChemokine CXCL2Cystic Fibrosis Transmembrane Conductance Regulatorcystic fibrosis transmembrane conductance regulator delta F508Interleukin-10LipopolysaccharidesMonokinesTumor Necrosis Factor-alpha

Identifiers

PMID17064416
PMCPMC1637104
OpenAlexW2105903244

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.