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IL-33/ST2 axis promotes the inflammatory response of nasal mucosal epithelial cells through inducing the ERK1/2 pathway.
Innate Immunity ( IF 3.2 ) Pub Date : 2020-05-26 , DOI: 10.1177/1753425920918911
Yun-Qiu Li 1 , Yu Zhong 1 , Xu-Ping Xiao 1 , Dan-Dan Li 1 , Zheng Zhou 1 , Yan-Yan Tian 2
Affiliation  

Allergic rhinitis (AR) is a nasal mucosal inflammatory disease mediated by environmental allergens. At present, the relationship between the IL-33/ST2 axis, ERK1/2 pathway and AR progression needs further exploration. In our study, an AR model was constructed in vitro by treating HNEpC cells with Der p1. qRT-PCR was applied to assess the mRNA levels of IL-33, ST2, TNF-α, IL-6, and IL-8. Western blotting was used to measure the protein levels of IL-33, ST2, and the downstream proteins p-ERK1/2, ERK1/2, p-RSK, and RSK. IL-6, IL-8, IL-33, and TNF-α protein levels in cell supernatants were evaluated by ELISA. Flow cytometry was performed to check cell apoptosis of HNEpC in the presence or absence of Der p1. Our results indicate that the relative levels of IL-33, ST2, TNF-α, IL-6, and IL-8 were increased significantly in the AR model group. The above effects were notably reversed after transfection with shIL-33 or shST2. IL-33 stimulation further resulted in the increase in both ST2 and inflammation-associated cytokines, and these effects were restored after shST2 treatment. Also, the levels of inflammatory factors induced by IL-33 stimulation or ST2 overexpression were reversed after applying an ERK1/2 pathway blocker. In conclusion, IL-33/ST2 mediated inflammation of nasal mucosal epithelial cells by inducing the ERK1/2 pathway.



中文翻译:

IL-33/ST2轴通过诱导ERK1/2通路促进鼻黏膜上皮细胞的炎症反应。

过敏性鼻炎(AR)是一种由环境过敏原介导的鼻黏膜炎症性疾病。目前,IL-33/ST2轴、ERK1/2通路与AR进展之间的关系有待进一步探索。在我们的研究中,在体外构建一个 AR 模型通过用 Der p1 处理 HNEpC 细胞。应用 qRT-PCR 来评估 IL-33、ST2、TNF-α、IL-6 和 IL-8 的 mRNA 水平。蛋白质印迹用于测量 IL-33、ST2 和下游蛋白质 p-ERK1/2、ERK1/2、p-RSK 和 RSK 的蛋白质水平。通过ELISA评估细胞上清液中的IL-6、IL-8、IL-33和TNF-α蛋白水平。进行流式细胞术以检查在存在或不存在 Der p1 的情况下 HNEpC 的细胞凋亡。我们的结果表明,AR模型组IL-33、ST2、TNF-α、IL-6和IL-8的相对水平显着增加。用 shIL-33 或 shST2 转染后,上述效果显着逆转。IL-33 刺激进一步导致 ST2 和炎症相关细胞因子的增加,并且这些影响在 shST2 治疗后恢复。还,应用 ERK1/2 通路阻滞剂后,IL-33 刺激或 ST2 过表达诱导的炎症因子水平逆转。总之,IL-33/ST2通过诱导ERK1/2通路介导鼻粘膜上皮细胞的炎症。

更新日期:2020-05-26
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