Prostaglandin E Receptor 2 (EP2) Dysregulation in Allergic Fungal Rhinosinusitis Nasal Polyp Epithelium

Prestina Smith-Davidson1,2, Khaled Altartoor2, M M Kabongo1,2

  • 1Sinonasal and Olfaction Program, National Institute on Deafness and Other Communication Disorders (NIDCD), NIH, Bethesda, Maryland, U.S.A.

The Laryngoscope
|November 2, 2024
PubMed
Abstract

Insights

Allergic fungal rhinosinusitis (AFRS) involves changes in nasal polyp gene expression. The study identified PTGER2 (prostaglandin E receptor 2) as a potential therapeutic target for AFRS.

Area of Science:

  • Otorhinolaryngology
  • Immunology
  • Genomics

Background:

  • Allergic fungal rhinosinusitis (AFRS) is an eosinophilic subtype of chronic rhinosinusitis with nasal polyposis (CRSwNP).
  • Understanding the molecular mechanisms of AFRS is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the transcriptome of nasal polyp epithelium in patients with AFRS.
  • To identify differentially expressed genes and potential therapeutic targets in AFRS.

Main Methods:

  • Sinonasal epithelial cells were obtained from healthy individuals and AFRS patients.
  • Cells were cultured using an air/liquid interface and analyzed via RNA-seq, RT-qPCR, immunoblotting, and immunocytochemistry.

Main Results:

  • Nineteen genes showed differential expression between healthy and AFRS epithelium.
  • Prostaglandin E receptor 2 (PTGER2) was significantly upregulated in AFRS and confirmed by multiple methods.
  • The EP2 receptor, encoded by PTGER2, was present in AFRS polyp epithelium.

Conclusions:

  • PTGER2 is a potential novel therapeutic target for AFRS.
  • EP2 receptor dysregulation may link AFRS to aspirin-exacerbated respiratory disease, suggesting shared disease pathways in severe CRSwNP.

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