The Characterization of IL-17A Expression in Patients with Chronic Rhinosinusitis with Nasal Polyps

Abstract

Interleukin (IL)-17A, mainly produced by Th17 cells, was previously described as an inflammatory cytokine that induces a profile of proinflammatory cytokines, chemokines, and metalloproteinases. Recent studies have revealed that IL-17 is correlated with inflammatory lung disorders by triggering an accumulation of neutrophils. More recently, we have shown that the expression of IL-17 may be involved in the development of nasal polyps (NPs). Here, we describe the characterization of IL-17 expression in patients with chronic rhinosinusitis with nasal polyps (CRSwNPs) from northeast China. Histopathological observations and immunohistochemical (IHC) staining for IL-17, IL-17RD, myeloperoxidase, and CD68 were performed on 52 specimens (42 NPs and 10 specimens of middle turbinate as normal control). Double IHC staining was performed to determine which cells expressed IL-17. The serum expression levels of IL-17 were determined by ELISA and the mRNA expression of IL-17 and Th17 cells transcription factor retinoid acid-related orphan receptor C (RORc) was determined by real-time quantitative polymerase chain reaction. 42.9% of CRSwNP specimens presented eosinophilic inflammation; 35.7% of CRSwNP specimens presented neutrophilic inflammation. Relatively higher mRNA expression levels of IL-17 and RORc were seen in CRSwNPs compared with the controls. A marked increase of IL-17 and IL-17RD proteins (p < 0.01) were seen in CRSwNP group. The expression levels of IL-17 and RORc did not differ between eosinophilic and noneosinophilic CRSwNPs (p > 0.05). However, high expression levels of IL-17RD were seen in noneosinophilic CRSwNPs compared with eosinophilic CRSwNPs (p < 0.05). The serum expression of IL-17 in CRSwNP patients was similar to healthy controls. The IL-17 expressing cells mainly were the macrophages as shown by double IHC staining. Chinese CRSwNP patients showed an enhanced Th17 response regardless of eosinophilic or noneosinophilic inflammation. IL-17 may be involved in the development of NPs through its local immune modulation.