Gong Guo-Qing, Ren Fang-Fang, Wang Yan-Jun, Wan Lang, Chen Shan, Yuan Jie, Yang Chuan-Mei, Liu Bang-Hua, Kong Wei-Jia
Department of Otolaryngology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Department of Otolaryngology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
J Huazhong Univ Sci Technolog Med Sci. 2017 Jun;37(3):412-418. doi: 10.1007/s11596-017-1749-1. Epub 2017 Jun 6.
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 CRSwNP 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.
鼻息肉(NP)是鼻腔和鼻窦常见的慢性炎症性疾病。尽管一些作者认为NP与白细胞介素(IL)-1β、IL-5、IL-8、粒细胞-巨噬细胞集落刺激因子(GM-CSF)、肿瘤坏死因子(TNF)-α和IL-17等炎症因子有关,但NP发病机制和进展的潜在机制仍不清楚。本研究调查了IL-17和syndecan-1在NP中的表达和分布,并探讨了这两种分子在嗜酸性粒细胞性慢性鼻-鼻窦炎伴鼻息肉(Eos CRSwNP)和非Eos CRSwNP发病机制中的作用。采用实时荧光定量聚合酶链反应(Real-time PCR)和免疫组织化学方法检测样本[NP、慢性鼻-鼻窦炎(CRS)患者的钩突(UP)以及垂体瘤手术健康对照者的中鼻甲(MT)]中IL-17和syndecan-1的表达。结果显示,NP和UP组织中IL-17和syndecan-1的表达水平均上调,但NP组织中的这两种因子均高于UP组织。Eos CRSwNP和非Eos CRSwNP样本的IL-17水平无显著差异,与Eos CRSwNP组织相比,非Eos CRSwNP组织中的syndecan-1水平升高。在所有组中,鼻黏膜上皮细胞、腺上皮细胞和炎症细胞中IL-17和syndecan-1的表达密切相关,提示IL-17和syndecan-1可能在非Eos CRSwNP的发病机制中发挥作用并相互作用。