Expression of IL-17 and Syndecan-1 in Nasal Polyps and Their Correlation with Nasal Polyps

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences 2017-06, Vol.37 (3), p.412-418
• Main Authors: Gong, Guo-qing, Ren, Fang-fang, Wang, Yan-jun, Wan, Lang, Chen, Shan, Yuan, Jie, Yang, Chuan-mei, Liu, Bang-hua, Kong, Wei-jia
• Format: Article
• Language: English
• Subjects: Case-Control Studies; Chronic Disease; colony; Correlation; Eosinophilia - genetics; Eosinophilia - immunology; Eosinophilia - pathology; Epithelial Cells - immunology; Epithelial Cells - pathology; Gene Expression Regulation; glandular; Humans; interleukin; Interleukin-17 - genetics; Interleukin-17 - immunology; macrophage; Medicine; Medicine & Public Health; mucosa; nasal; Nasal Cavity - immunology; Nasal Cavity - pathology; Nasal Mucosa - immunology; Nasal Mucosa - pathology; Nasal Polyps - complications; Nasal Polyps - genetics; Nasal Polyps - immunology; Nasal Polyps - pathology; pathogenesis; polyp; Rhinitis - complications; Rhinitis - genetics; Rhinitis - immunology; Rhinitis - pathology; rhinosinusitis; Sinusitis - complications; Sinusitis - genetics; Sinusitis - immunology; Sinusitis - pathology; Syndecan-1 - genetics; Syndecan-1 - immunology
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-017-1749-1

Nasal polyp（NP） is a common chronic inflammatory disease of the nasal cavity and sinuses. Although some authors have suggested that NP is related to inflammatory factors such as interleukin（IL）-1β, IL-5, IL-8, granulocyte-macrophage colony-stimulating factor（GM-CSF）, tumor necrosis factor（TNF）-α, and IL-17, the mechanisms underlying the pathogenesis and progression of NP remain obscure. This study investigated the expression and distribution of IL-17 and syndecan-1 in NP, and explored the roles of these two molecules in the pathogenesis of eosinophilic chronic rhinosinusitis with nasal polyps（Eos CRSwNP） and non-Eos CRSwNP. Real-time PCR and immunohistochemistry were used to detect the expression of IL-17 and syndecan-1 in samples [NP, unciform process（UP） from patients with CRS, and middle turbinate（MT） from healthy controls undergoing pituitary tumor surgery]. The results showed that the expression levels of IL-17 and syndecan-1 were upregulated in both NP and UP tissues, but both factors were higher in NP tissues than in UP tissues. There was no significant difference in IL-17 levels between the Eos CRSw NP and non-Eos CRSwNP samples, and syndecan-1 levels were increased in the non-Eos CRSwNP tissues as compared with those in Eos CRSwNP tissues. In all of the groups, there was a close correlation between the expression of IL-17 and syndecan-1 in nasal mucosa epithelial cells, glandular epithelial cells, and inflammatory cells, suggesting that IL-17 and syndecan-1 may play a role, and interact with each other, in the pathogenesis of non-Eos CRSwNP.