Interaction of thymic stromal lymphopoietin, IL-33, and their receptors in epithelial cells in eosinophilic chronic rhinosinusitis with nasal polyps
Interaction of thymic stromal lymphopoietin, IL-33, and their receptors in epithelial cells in eosinophilic chronic rhinosinusitis with nasal polyps
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嗜酸性慢性鼻窦炎伴鼻息肉中胸腺基质淋巴细胞生成素、IL-33及其上皮细胞受体的相互作用
DOI：
10.1111/all.12667
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发表时间：
2015-09-01
期刊：
影响因子：
12.4
通讯作者：
Liu, Z.
中科院分区：
文献类型：
--
作者：
Liao, B.;Cao, P. -P.;Liu, Z.
胸腺基质淋巴细胞生成素（TSLP）、IL-25和IL-33系统参与Th 2应答的启动和发展。本研究旨在探讨TSLP、IL-25、IL-33及其受体在慢性鼻窦炎伴鼻息肉（CRSwNPs）患者鼻黏膜上皮细胞（HNECs）中参与2型辅助性T细胞（Th）应答的作用及其相互关系。流式细胞术检测TSLP/共同型TSLP受体（TSLPR）/IL-7受体（IL-7 R）、IL-25/IL-17 B受体（IL-17 RB）、IL-33/膜结合ST 2（ST 2L）/可溶性ST 2（sST 2）。HNECs培养在空气-液体界面被用来探索这些细胞因子systems.ResultsCompared相比，控制和noneosinophilic CRSwNP，表达TSLP/TSLPR/IL-7 R和ST 2 L/sST 2的表达显着增加嗜酸性CRSwNP，主要是在上皮细胞。相比之下，与对照组相比，嗜酸性和非嗜酸性CRSwNP中的上皮细胞中IL-33和IL-25/IL-17 RB的表达增强。TSLP、TSLPR和ST 2L的表达与嗜酸性CRSwNP的症状和计算机断层扫描评分以及鼻窦粘膜中Th 2细胞因子的表达正相关。ST 2L的表达与TSLP及其受体的表达相关。TSLP可诱导HNECs表达ST 2L，ST 2L促进IL-33诱导的TSLP表达。Th 1/Th 17细胞因子可上调HNECs. ConclusionsTSLP、IL-33及其受体与Th 2细胞因子之间的正反馈环可能促进嗜酸性粒细胞CRSwNP的Th 2偏向性炎症。
BackgroundThymic stromal lymphopoietin (TSLP), IL-25, and IL-33 system contribute to the initiation and development of Th2 responses. This study aimed to explore the involvement of TSLP, IL-25, IL-33, and their receptors in type 2 T-helper (Th) responses in chronic rhinosinusitis with nasal polyps (CRSwNPs) and their cross-regulation in human nasal epithelial cells (HNECs).MethodsImmunohistochemistry, quantitative RT-PCR, ELISA, Bio-Plex assay, and flow cytometry were used to detect the expression of TSLP/common -like TSLP receptor (TSLPR)/IL-7 receptor (IL-7R), IL-25/IL-17B receptor (IL-17RB), and IL-33/membrane-bound ST2 (ST2L)/soluble ST2 (sST2) in sinonasal mucosa and HNECs. HNECs cultured at an air-liquid interface were used to explore the expression in regulation of these cytokine systems.ResultsCompared with controls and noneosinophilic CRSwNP, the expression of TSLP/TSLPR/IL-7R and ST2L/sST2 was significantly increased in eosinophilic CRSwNP, predominantly in epithelial cells. In contrast, the expression of IL-33 and IL-25/IL-17RB was enhanced in epithelial cells in both eosinophilic and noneosinophilic CRSwNP compared to controls. The expression of TSLP, TSLPR, and ST2L was positively correlated with symptom and computer tomography scan scores in eosinophilic CRSwNP and with Th2 cytokine expression in sinonasal mucosa. The expression of ST2L was correlated with TSLP and its receptor expression. TSLP could induce ST2L expression that promoted IL-33-induced TSLP expression in HNECs. In addition, TSLP/TSLPR/IL-7R and ST2L could be induced by Th2 cytokines, while IL-25/IL-17RB and IL-33 could be upregulated by Th1/Th17 cytokines, in HNECs.ConclusionsThe positive feedback loop between TSLP, IL-33 and their receptors, and Th2 cytokines may facilitate Th2-skewed inflammation in eosinophilic CRSwNP.