Evidence map›Paper›PMID 39276033›Full record

ArticleThe Laryngoscope2025

Azithromycin Prevents Subglottic Stenosis in Mice.

Daniel D Ghaderi, Matthew R Aronson, Amrita Mehta, Ryan M Friedman, Kendra S McDaid, Terri Giordano, Ian N Jacobs, Riccardo Gottardi

Abstract read
In one paragraph

Article in The Laryngoscope, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Inhibition of the MRTF-A/SRF signaling axis alleviates vocal fold scarring.Matrix biology : journal of the International Society for Matrix Biology · 2025
    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

8 authors.

Daniel D GhaderiDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Matthew R AronsonDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, USA.ORCID 0000-0002-8871-8265
Amrita MehtaDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Ryan M FriedmanDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Kendra S McDaidDepartment of Veterinary Resources, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Terri GiordanoDivision of Otolaryngology, Department of Surgery, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Ian N JacobsDivision of Otolaryngology, Department of Surgery, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Riccardo GottardiDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, USA.ORCID 0000-0001-8040-5531

Funding

Children's Hospital of PhiladelphiaFrontier Program in Airway Disorders of the Children's Hospital of PhiladelphiaNational Science Foundation Graduate Research Fellowship Program DGE 1845298
6 · The paper itself

Abstract

objectivePediatric subglottic stenosis (SGS) is characterized by subglottic narrowing which occurs when pathological fibroblasts deposit extracellular matrix that reduces airway patency. Recent clinical observations have suggested that azithromycin may have favorable impacts on SGS reduction while treating airway infections; furthermore, our recent work in mice demonstrated that the airway microbiome influences SGS. In this work, we characterize the protective effect of azithromycin as an immunomodulatory and antibacterial therapeutic against subglottic stenosis.

methodsImmunomodulatory and antifibrotic effects of azithromycin were assessed on TGF-β1-stimulated airway fibroblasts at 10 μg/mL for 5 days. Changes in gene expression were quantified by RT-qPCR and myofibroblast differentiation by α-SMA immunostaining. Murine airways were pretreated (2-weeks) with intranasal azithromycin before SGS injury by a twisted wire brush. Disease severity and immune response were characterized by histology and immunostaining for immune cells.

resultsIn vitro, azithromycin treatment of TGF-β1-stimulated fibroblasts exhibited strong reductions in extracellular matrix (COL1A1, LOX) and myofibroblast-related gene expression (ACTA2). Notably, there was a significant reduction in pro-fibrotic expression, which was observed with 10 μg/mL azithromycin. Immunostaining of fibroblasts for α-SMA revealed strong reductions in the number of positive-staining cells and the intensity of each positive cell. In vivo, azithromycin exhibited a significant decrease in lamina propria thickness indicative of reduced stenosis with associated changes in T-cell infiltration.

conclusionsOverall, we show azithromycin prevents pro-fibrotic gene expression and myofibroblast differentiation and can help protect mice from developing SGS. This introduces azithromycin as a potential treatment for SGS. LEVEL OF EVIDENCE: NA Laryngoscope, 135:409-415, 2025.

Indexed as

Anti-Bacterial AgentsAzithromycinDisease Models, AnimalLaryngostenosisAnimalsFibroblastsMiceMice, Inbred C57BLMyofibroblastsTransforming Growth Factor beta1Anti-Bacterial AgentsAzithromycinTransforming Growth Factor beta1antibioticsfibroblastspediatricT cells

Identifiers

PMID39276033
PMCPMC11635149

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LicenceCC BY-NC-ND
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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.