Regulation and expression of IL-32 in chronic rhinosinusitis

Background 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. Methods 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. Results 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. Conclusion 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.