CRSwNP initiation, not always an interleukin fault
Reviewed by Hassan Mohammed

CRSwNP, similar to asthma, is an inflammatory disorder (type II) with eosinophilia and raised IL-5 and IL-13. Inflammation in CRSwNP is thought to be started by IL-25, IL-33 and thymic stromal lymphopoietin (TSLP), all of which form an important part of type II immunity and type II inflammation response. Mucosa from 46 patients with Samter’s Triad and of 34 healthy controls were assessed for levels of IL-25, IL-33 and TSLP using four different methods, including PCR and western blot. There was no significant difference in IL-25 and IL-33 levels between patients and controls. However, TSLP levels were significantly different. The authors concluded, based on the available literature, that the mechanism of CRSwNP initiation might be different between Asian countries in which IL-25 and IL-33 seem to be involved, and Western countries in which TSLP appears to be the main factor. This study adds to the evidence showing how variable and multifactorial CRSwNP is. Such variability might lead to problems in targeted therapies. It is worth noting that this study was mainly on patients with Samter’s triad which might help explain the difference from the existing literature.

Epithelial activators of type 2 inflammation: Elevation of thymic stromal lymphopoietin, but not IL‐25 or IL‐33, in chronic rhinosinusitis with nasal polyps in Chicago, Illinois.
Ogasawara N, Klingler AI, Tan BK, et al.
ALLERGY
2018;73(11):2251-4.