Evidence map›Paper›PMID 37660113›Full record

ArticleScientific reports2023

Azithromycin promotes proliferation, and inhibits inflammation in nasal epithelial cells in primary ciliary dyskinesia.

Zofia Varenyiova, Laura S Rojas-Hernandez, Jacquelyn Spano, Vaclav Capek, Yael Rosenberg-Hasson, Tyson Holmes, Carlos Milla

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Utilising human cellular models of primary ciliary dyskinesia: a scoping review.European respiratory review : an official journal of the European Respiratory Society · 2026
    Article
  3. Preclinical human models of primary ciliary dyskinesia.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  4. [Report of 24 cases of primary ciliary dyskinesia in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. 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

7 authors at 3 institutions in 2 countries.

Zofia VarenyiovaDepartment of Pediatrics, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic. z.varenyiova@gmail.com.
Laura S Rojas-HernandezCenter for Excellence in Pulmonary Biology, Stanford University, Palo Alto, CA, USA.
Jacquelyn SpanoCenter for Excellence in Pulmonary Biology, Stanford University, Palo Alto, CA, USA.
Vaclav CapekDepartment of Pediatrics, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
Yael Rosenberg-HassonHuman Immune Monitoring Center, Stanford University, Stanford, CA, USA.
Tyson HolmesHuman Immune Monitoring Center, Stanford University, Stanford, CA, USA.
Carlos MillaCenter for Excellence in Pulmonary Biology, Stanford University, Palo Alto, CA, USA.
Center for Excellence in Education · USCharles University · CZStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary ciliary dyskinesia (PCD) is a genetic disorder associated with recurrent and chronic respiratory infections due to functional defects of motile cilia. In this study, we aimed to elucidate inflammatory and proliferative responses in PCD respiratory epithelium and evaluate the effect of Azithromycin (AZT) on these responses. Airway basal cells (BCs) were isolated from nasal samples of Wild-type (WT) epitope of healthy donors and PCD donors with bi-allelic mutations in DNAH5, DNAH11 and CCDC39. Cells were expanded in vitro and stimulated with either Lipopolysaccharide (LPS) or vehicle control. Post stimulation, cells were treated with either Azithromycin (AZT) or vehicle control. Cell proliferation was imaged in real-time. Separately, BCs from the same donors were expanded and grown at an air-liquid interface (ALI) to generate a multi-ciliated epithelium (MCE). Once fully mature, cells were stimulated with LPS, AZT, LPS + AZT or vehicle control. Inflammatory profiling was performed on collected media by cytokine Luminex assay. At baseline, there was a significantly higher mean production of pro-inflammatory cytokines by CCDC39 BCs and MCEs when compared to WT, DNAH11 and DNAH5 cells. AZT inhibited production of cytokines induced by LPS in PCD cells. Differences in cell proliferation were noted in PCD and this was also corrected with AZT treatment.

Indexed as

AzithromycinCiliary Motility DisordersCell ProliferationCytokinesEpithelial CellsHumansInflammationLipopolysaccharidesAzithromycinCytokinesLipopolysaccharides

Identifiers

PMID37660113
PMCPMC10475097
OpenAlexW4386387613

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.