The role of Hypoxia and lymphangiogenesis in nasal polyposis

Hypoxia creates a microenvironment conducive to polypogenesis by regulating immune responses of the nasal polyp (NP) epithelium. Three groups of tissue samples were collected: inferior turbinate (IT) and NP from individuals with chronic rhinosinusitis with NPs (CRSwNP), and control IT. A positive relationship was detected between HIF1α, HIF2α protein expression in epithelial cells and endoscope score in NP samples, while there was a negative correlation between HIF1α expression and degree of eosinophil infiltration. Enzyme-linked immunosorbent assays demonstrated decreased IL-17A expression upon prolonged exposure to hypoxia in both IT and NP samples from patients with CRSwNP, while IL-17A increased in control IT epithelial cells; correlation and time-dependency were observed between HIF1α and IL-17A expression in both IT and NP samples from patients with CRSwNP. These observations suggest that hypoxia is involved in the pathogenesis of NPs through regulation of IL-17A secretion and HIF1α and HIF2α expression in the NP epithelium. The microvessel density (MVD), lymph vessel density (LVD) and microvessel pericyte coverage index (MPI), were assessed and correlated with the degree of edema by measuring albumin expression. MVD expression was not significantly higher in NPs than that in the control group (p > 0.05) but MPI was significantly lower in NPs than that in the control group (p < 0.05). We suppose that lymphangiogenesis may play crucial roles in the evolution of NPs and hypoxia may be the first key step of signal transduction of polyp epithelium in polyposis.

Publication History

Publication Date:
18 April 2018 (online)