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Updated: Jun 8, 2025

Author Spotlight: Advancing Allergic Rhinitis Research with Multicolor Immunofluorescence
Published on: September 22, 2023
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.
Objectives:
Allergic fungal rhinosinusitis (AFRS) is an eosinophilic subtype of chronic rhinosinusitis with nasal polyposis (CRSwNP). This study aimed to investigate the transcriptome of AFRS nasal polyp epithelium.
Methods:
Sinonasal epithelial cells were harvested from healthy nasal mucosa and polyp tissue collected from participants undergoing elective sinonasal surgery. Primary epithelial cells were subsequently grown in air/liquid interface and subjected to RNA-seq analysis, RT-qPCR, immunoblotting, and immunostaining.
Results:
A total of 19 genes were differentially expressed between healthy and AFRS sample epithelium. The second top candidate gene, ranked by adjusted p-value, was prostaglandin E receptor 2 (PTGER2). The upregulation of PTGER2 was confirmed by RT-qPCR and immunoblot. The presence of the EP2 receptor, encoded by the PTGER2 gene, was confirmed by immunocytochemistry.
Conclusion:
PTGER2 is a potential novel therapeutic target for AFRS. EP2 dysregulation is associated with aspirin-exacerbated respiratory disease, potentially giving insight into common mechanisms of disease in severe CRSwNP.
Level Of Evidence:
NA Laryngoscope, 135:S1-S8, 2025.
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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