IL-33 has a nuclear distribution and is not increased in peripheral lung of COPD patients

Interleukin-33 (IL-33), a member of the IL-1 cytokine family, is crucial for induction of Th2-type immune responses but is also involved in the induction of non-Th2-type inflammation as a pro-inflammatory cytokine, similar to IL-1 and IL-18. The aim of our study was to investigate by immunohistochemistry (IHC), RT-qPCR, ELISA and Western blotting (WB) the expression and the amount of IL-33 in peripheral lung, and bronchoalveolar lavage (BAL) from 15 age- and smoking history-matched smokers with normal lung function and 15 smokers with mild to moderate stable COPD not treated with ICS and/or theophylline. The IHC staining was mainly confined to the nuclei of endothelial cells and small airway epithelial cells. The number of IL-33 positive cells and the level of mRNA expression was not significantly different in patients with COPD compared to controls. IL-33 was under detection limits using ELISA (BAL) and WB (peripheral lung). These data suggest that an IL-33-mediated immune response, may not be critical in COPD and its nuclear role is uncertain.