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.