ABSTRACT
The introduction of topically administered glucocorticoids has improved the treatment of upper [rhinitis, nasal polyps (NP)] and lower (asthma) airway inflammatory disease. The clinical efficacy of glucocorticoids may depend in part on their ability to reduce airway eosinophil infiltration by preventing their increased viability and activation. Both topical and systemic glucocorticoids may affect eosinophil function by both directly reducing eosinophil viability and activation (1-4) or by indirectly reducing the secretion of chemotactic cytokines by nasal mucosa and polyp epithelial cells (5-8). The potency of these effects is lower in nasal polyps than in nasal mucosa suggesting an induced inflammatory resistance to steroid treatment in chronic rhinosinusitis (CRS)/nasal polyposis (4,6).
