Corticosteroids
For many years, corticosteroids have been considered a mainstay of treatment for CRS. Corticosteroids have potent anti-inflammatory properties and suppress T2 inflammation greater than T1 and T3, possibly explaining their better efficacy in CRSwNP than CRSsNP138-141. In the case of T2 inflammation, corticosteroids suppress ILC2 cells, Th2 cells, basophils and eosinophils 142-145. Neutrophils are relatively resistant to corticosteroid effects, however 146,147. Reduced activity against T3 inflammation may explain the decreased corticosteroid responsiveness observed in clinical trials of Asian CRSwNP as well as CRSsNP in general versus Western CRSwNP66,147-154. Topical corticosteroid sprays have limited access to inflamed sinus tissue but high-volume steroid irrigations, improved delivery devices and steroid-impregnated implants have improved efficacy 155-160. Epithelial barrier remodeling defects and basal cell hyperplasia induced by T2 inflammation are partially reversed by corticosteroids 161,162. Barrier defects may reflect expansions of basal epithelial cells due to epigenetically determined events in T2 CRS and may increase antigen access, heightening inflammation 46,112,163.