Regulation and expression of IL‐32 in chronic rhinosinusitis

Abstract

Activated T lymphocytes and their interaction with resident tissue cells, particularly epithelium, play important roles in inflammatory processes in chronic rhinosinusitis (CRS). IL-32 is a recently described cytokine, which is expressed in a variety of tissue cells and involved in the pathogenesis of several chronic inflammatory diseases. Human sinus epithelial cells were isolated from biopsies and stimulated with different cytokines, which play a role in the pathogenesis of CRS. IL-32 mRNA expression was analyzed using real-time-PCR, IL-32 protein was determined by Western blot and flow cytometry as well as immunofluorescent staining in primary sinus epithelial cells and nasal biopsies from patients with CRS and healthy controls. IL-32 mRNA was upregulated by TNF-α and IFN-γ in primary sinus epithelial cells, whereas IL-1 β, IL-4, IL-13, and IL-17 did not influence IL-32 expression. IL-32 mRNA expression was significantly higher in human primary sinonasal epithelial cells (HSECs) cocultured with Th1 cells compared with HSECs cocultured with Th0 or Th2 cells. IL-32 mRNA expression was significantly higher in biopsies from sinus epithelial tissue of CRS patients with nasal polyps compared with healthy subjects (P = 0.01). IL-32 was detected in biopsies from patients with CRS, whereas it was scarcely present in control tissues. The induction of IL-32 by TNF-α, IFN-γ and Th1 cells as well as its increased expression in sinus tissues from CRS patients with nasal polyps demonstrated a potential role for IL-32 in the pathogenesis of CRS.