Synergistic relationship between TSLP and IL‐33/ST2 signaling pathways in allergic rhinitis and the effects of hypoxia

胸腺基质淋巴细胞生成素 医学 免疫学 免疫印迹 鼻粘膜 白细胞介素33 免疫系统 间质细胞 细胞凋亡 缺氧(环境) 分泌物 免疫组织化学 信号转导 白细胞介素 细胞因子 癌症研究 细胞生物学 生物 内分泌学 化学 基因 有机化学 生物化学 氧气
作者
Ruofei Huang,Wei Mao,Guoliang Wang,Jian Ding,Ying Sun,Gang Gao,Ping Dong,Zhenfeng Sun
出处
期刊:International Forum of Allergy & Rhinology [Wiley]
卷期号:10 (4): 511-520 被引量:20
标识
DOI:10.1002/alr.22504
摘要

Background The World Health Organization (WHO) has noted that allergic diseases are a major health problem of the 21st century. Allergic rhinitis (AR) is a type I allergic disease characterized by nasal mucosa and immune system abnormalities. AR is mediated by various inflammatory cells and is mainly characterized by altered secretion of cytokines. Thymic stromal lymphopoietin (TSLP) and the interleukin‐33/stimulation‐expressed gene 2 (IL‐33/ST2) signaling pathway are cytokines that play pivotal roles in many inflammatory responses and allergic reactions. There have been reports of interactions between the 2 pathways in many diseases. Hypoxia is a common pathologic manifestation of AR. The aim of this study was to explore the relationship and expressions and biologic functions of TSLP and IL‐33/ST2 in AR, and also to determine the effects of hypoxia on these cytokines. Methods The rat nasal mucosal epithelium was obtained from Wistar rats. Cells were cultured in groups under hypoxia and normoxia conditions. Identification of rat nasal epithelial cell (RNEpC) and protein expressions was done by immunohistochemistry and immunofluorescence methods. Cell proliferation and migration were examined using the cell counting kit‐8 (CCK‐8) and Transwell kit. Detection of apoptosis was tested using a fluorescence apoptosis kit. Enzyme‐linked immunoassay (ELISA) and Western blot analysis ELISA were used to measure cell secretion and protein expressions. For these experiments, TSLP was knocked down by lentivirus transfection and IL‐33 blocked with its antagonist. Results TSLP, IL‐33, and ST2 expressions were significantly higher in nasal mucosa epithelial cells from AR rats than in those from control rats. Hypoxia further promoted their expression. Increased TSLP and IL‐33/ST2 promoted cell proliferation, inhibited cell apoptosis, and enhanced cell migration. In addition, the downregulation of TSLP expression effectively attenuated expression of the IL‐33/ST2 axis and, through use of IL‐33 antagonists, could also reduce TSLP expression, a synergistic effect more obvious under hypoxia. Conclusion Our data indicate that TSLP and IL‐33/ST2 signaling pathways interact with each other in the pathogenesis and pathologic development of AR. TSLP inhibition is a key factor in AR treatment. Inhibiting hypoxia‐induced pathologic processes could represent a therapeutic effect by inhibiting IL‐33/ST2 expression via downregulating TSLP.
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