The role of YKL40 in the pathogenesis of CRS with nasal polyps.

Abstract

Many Chinese patients who experience chronic rhinosinusitis with nasal polyps (CRSwNP) have been shown to exhibit specifically enhanced TH1/TH17 responses and excessive neutrophil accumulation without demonstrating significant eosinophilia. These patients may be subject to different pathologies and therapies compared to Western patients. YKL40 can be produced by neutrophil and is associated with many inflammatory diseases, while its role in the pathogenesis of chronic rhinosinusitis (CRS) has yet to be determined. The aim of this study was to investigate the relationship between the expression level and biologic role of YKL40 in CRS. YKL40 expression was examined via quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), immunohistochemistry, and Western blot. Human nasal epithelia cells (HNECs) were isolated to detect YKL40 expression in response to specific inflammatory stimulation. YKL40 expression levels were significantly higher in NP patients compared to the turbinates of CRSsNP/CRSwNP and the control group and can be strongly activated by stimulation with IL-4 in vitro and suppressed by the other pro-inflammatory cytokines; lipopolysaccharide (LPS) and dexamethasone also caused significant decreases in YKL40 expression in HNECs. YKL40 may play a significant role in Chinese patients with CRSwNP. The molecular mechanisms identified here may aid in the design of new therapeutic strategies for improving the clinical outcomes of Chinese patients.