Hypoxia regulates IL-17A secretion from nasal polyp epithelial cells

Area of Science:

• Immunology
• Pathophysiology
• Otolaryngology

Background:

• Nasal polyps (NPs) are associated with chronic rhinosinusitis.
• Hypoxia is implicated in polypogenesis by modulating immune responses in the nasal polyp epithelium.

Purpose of the Study:

• To investigate the immunocompetence of nasal polyp (NP) and control epithelial cells under hypoxic conditions.
• To explore the relationship between hypoxia, immune responses, and polypogenesis.

Main Methods:

• Collected tissue samples from inferior turbinate (IT) and NP of patients with chronic rhinosinusitis with NPs (CRSwNP) and controls.
• Cultured primary human nasal epithelial cells under hypoxic and normoxic conditions.
• Analyzed protein expression (HIF1α, HIF2α) and IL-17A levels using ELISA and correlated with clinical scores and eosinophil infiltration.

Main Results:

• Positive correlation between HIF1α/HIF2α expression and endoscope score in NP samples.
• Negative correlation between HIF1α expression and eosinophil infiltration.
• Decreased IL-17A expression in NP and CRSwNP IT epithelial cells under hypoxia, contrasting with increased IL-17A in control IT cells.
• Observed correlation and time-dependency between HIF1α and IL-17A expression in CRSwNP samples.

Conclusions:

• Hypoxia plays a role in nasal polyp pathogenesis.
• Hypoxia regulates IL-17A secretion and HIF1α/HIF2α expression in the NP epithelium, contributing to polyp formation.