Mechanisms and pathogenesis of chronic rhinosinusitis

Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by local inflammation of the upper airways and is historically divided into 2 main phenotypes: CRS with nasal polyps and CRS without nasal polyps. Inflammation in CRS is mainly characterized by 3 endotypes based on elevation of canonical lymphocyte cytokines: type (T) 1 (T1) by T(H)1 cytokine IFN-gamma, T2 by T(H)2 cutokines IL-4, IL-5, and IL-13, and T3 by T(H)17 cytokines including IL-17. Inflammation in both CRS without nasal polyps and CRS with nasal polyps is highly heterogeneous, and the frequency of various endotypes varies geographically around the world. This finding complicates establishment of a unified understanding of the mechanisms of pathogenesis in CRS. Sinonasal epithelium acts as a passive barrier, and epithelial barrier dysfunction is a common feature in CRS induced by endotype-specific cytokines directly and indirectly. The sinonasal epithelium also participates in both innate immunity via recognition by innate pattern-recognition receptors and promotes and regulates adaptive immunity via release of chemokines and innate cytokines including thymic stromal lymphopoietin. The purpose of this review was to discuss the contribution of the epithelium to CRS pathogenesis and to update the field regarding endotypic heterogeneity and various mechanisms for understanding pathogenesis in CRS.

Automated summary

Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by inflammation in the upper airways, which can be divided into two main types based on the presence of nasal polyps. The inflammation is characterized by three different endotypes based on the elevation of specific cytokines. The sinonasal epithelium plays a crucial role in the pathogenesis of CRS by acting as a barrier and participating in both innate and adaptive immunity. Further research is needed to fully understand the mechanisms of CRS pathogenesis.