ArticleFrontiers in immunology2021
Persistent Inflammation and Nitric Oxide Dysregulation Are Transcriptomic Blueprints of Subglottic Stenosis.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Preclinical Vocal Fold and Airway Injury Models: A Scoping Review.Laryngoscope investigative otolaryngology · 2025Review
- Review
- NOS2 and COX-2 Co-Expression Promotes Cancer Progression: A Potential Target for Developing Agents to Prevent or Treat Highly Aggressive Breast Cancer.International journal of molecular sciences · 2024Review
- Amelioration of Subglottic Stenosis by Antimicrobial Peptide Eluting Endotracheal Tubes.Cellular and molecular bioengineering · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subglottic stenosis (SGS) is a recurrent, obstructive, fibroinflammatory disease of the upper airway resulting in severe dyspnea, dysphonia, as well as other potentially fatal complications. Although aberrant inflammation and wound-healing are commonly associated with pathogenesis, the mechanism through which such processes occur and recur in affected patients remains poorly studied. Here we report that transcriptomic profiling of laryngotracheal regions from minimally-invasive mucosal swabs of SGS patients reveals a distinctively pro-inflammatory gene signature. Surprisingly, comparative genomics between SGS patients and mice with direct laryngotracheal injury suggest that SGS patients bear more resemblance to the acute than chronic phase of injury. Furthermore, functional and regulatory network analyses identify neutrophilic involvement through hyper-activation of NF-κB and its downstream inflammasome as a potential master regulator. Interestingly, nitric oxide synthesis was found to be downregulated in SGS patients compared to healthy controls. Thus, SGS represents a state of immunodeficiency whereby defective immune clearance triggers recurrent, long-lasting production of pro-inflammatory cytokines.
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