Clinical Report: The Role of the Alarmin–ILC2 Pathway in Chronic Olfactory Impairment
Background
Allergic rhinitis (AR) is a prevalent inflammatory condition that significantly impacts quality of life and is associated with olfactory dysfunction (OD). Current understanding suggests that while conductive obstruction is a common cause of OD in AR, some patients experience persistent smell loss despite improved nasal congestion, indicating the potential involvement of additional sensorineural mechanisms.
Data Highlights
No numerical data or trial data presented in the article.
Key Findings
AR is associated with olfactory dysfunction, affecting 28%-43% of patients.
Persistent OD in AR may not solely be due to conductive obstruction.
Alarmin–ILC2 pathway activation may contribute to AR-associated OD.
IL-33 and TSLP released from epithelial cells may engage ILC2s in the olfactory cleft.
Current evidence is primarily indirect and derived from animal models and other inflammatory conditions.
Clinical Implications
Clinicians should consider the potential for underlying inflammatory mechanisms in patients with persistent olfactory dysfunction.
Conclusion
The proposed model of the alarmin–ILC2 pathway in AR-associated OD presents a framework for future research.
A cross-sectional metagenomic study found greater oral microbiome richness among adults with chronic rhinosinusitis, particularly nonallergic chronic rhinosinusitis, while associations with asthma, airway inflammation, and most lung-function measures were inconsistent.
