Inflammatory mechanisms and remodeling in chronic rhinosinusitis and nasal polyps

Abstract

Chronic rhinosinusitis (CRS) is presently classified into two subgroups: CRS without and CRS with nasal polyps. A variety of inflammatory mediators, including cytokines and chemokines, as well as adhesion molecules and matrix metalloproteinases, are upregulated in both subgroups of CRS; remodeling is also observed in both. However, there are also characteristic differences. Whereas CRS without nasal polyps has more neutrophilic infiltration, in CRS with nasal polyps (especially when associated with allergy/asthma) eosinophil infiltration is strikingly increased. Although several features of remodeling (eg, squamous metaplasia, basement membrane thickening, collagen deposition, hyperplasia of mucous glands, and goblet cells) are features seen in both subgroups of CRS, epithelial shedding as observed in asthma is not seen in either subgroup. Furthermore, pseudocyst formation seen in CRS with nasal polyps is not seen in CRS without nasal polyps.