Repurposing celecoxib ameliorates olfactory dysfunction following rhinosinusitis by attenuating neuroinflammation

Rhinosinusitis disrupts the neuroepithelium, promotes inflammatory cell infiltration, and ultimately leads to olfactory dysfunction. Celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, reduces neuroinflammation through its antiinflammatory effects. We hypothesize that celecoxib can mitigate sensorineural olfactory impairment by reducing inflammation, preserving neuroepithelial structure, and exerting neuroprotective effects.

Male C57BL/6 mice were intranasally administered lipopolysaccharide (LPS) for three weeks to induce rhinosinusitis. Celecoxib treatment was also administered via subcutaneous injection. The mice then underwent histological staining in sinonasal tissue, olfactory function test, and quantitative genomic expression patterns in the olfactory bulb.

Following intranasal administration of LPS, mice exhibited impaired olfactory function, increased neutrophil infiltration, an elevated number of goblet cells in the sinonasal mucosa, and upregulated mRNA expression of inflammatory markers indicative of neuroinflammation in the olfactory bulb. Celecoxib treatment resulted in improved olfactory function, reduced neutrophil infiltration, decreased goblet cells number, and attenuated neuroinflammation in the olfactory bulb.

These findings suggest that celecoxib alleviates sensorineural olfactory dysfunction by reducing sinonasal neuroinflammation, highlighting its therapeutic potential in rhinosinusitis-associated olfactory loss.