[Role of IL-33 in bronchial asthma].

IL-33 is a member of the IL-1 family and has been identified as an agonist of ST2L. IL-33 drives the production of Th2-associated cytokines and IgE, and IL-33 administration induces eosinophilia and hypertrophy of bronchial epithelial cells, as well as mucus secretion in vivo. Such changes resemble pathological findings in bronchial asthma (BA). In this study, we investigated the relationship between IL-33 and BA by evaluating serum IL-33 levels. Serum was obtained from BA patients (n = 20), emphysema patients (n = 5) and from non-smoking healthy controls (n = 8). IL-33 levels were assayed by enzyme-linked immunosorbent assay. Then, we divided BA patients according to 5 factors; (1) IgE concentration, (2) eosinophil count, (3) current treatment, (4) classification of severity, and (5) smoking status. Atopic BA patients showed significantly higher IL-33 levels than non-atopic patients. IL-33 was significantly higher in untreated patients, and in the moderate and severely affected groups. Smoking BA and emphysema patients had lower levels than nonsmoking BA patients. Eosinophil counts were not related to IL-33 levels. The present study suggests that IL-33 is closely associated with IgE levels and the exacerbation of BA. We speculated that IL-33 elevation is responsible for the maintenance of airway inflammation and hypersensitivity. It is possible that low IL-33 levels in smokers are caused by the deterioration of the airway epithelium and endothelium.