This study aimed to explore the effect of Sgk1 on Th9 differentiation and the underlying mechanism in asthma. The asthmatic mouse model induced by ovalbumin (OVA) and CD4+T cells which were cultured with TGF-β, IL-2, IL-4, and anti-IFN-γ were applied in vivo and in vitro, respectively. Flow cytometry, quantitative real-time PCR (qRT-PCR), and ELISA were performed to detect T-helper 9 (Th9) cells, IL-9 expression, and IL-9 release. Western blot was performed to examine phosphorylated(p)-IKKα, p-IκBα, p-p65, and IRF4 levels. Hematoxylin/eosin (H&E) staining was adopted to assess pathological changes of lung tissues. Inhibition of Sgk1 dramatically reversed elevated Th9 cells and IL-9 expression in the lung tissues of asthmatic mice. In vitro, Sgk1 promoted Th9 differentiation and elevated p-IKKα, p-IκBα, p-p65, and IRF4 levels, but inhibition of IKKα/IκBα/p65 pathway and IRF4 both reversed enhanced Th9 differentiation by Sgk1. Sgk1→IKKα/IκBα/NF-κBp65→IRF4→Th9 axis may be implicated in asthma development.

中文翻译：

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SGK1通过NF-κB信号通路在哮喘中增强Th9细胞分化和气道炎症

本研究旨在探讨Sgk1对Th9分化的影响及其在哮喘中的潜在机制。分别在体内和体外应用卵清蛋白（OVA）和CD4+T细胞诱导的哮喘小鼠模型，该细胞与TGF-β、IL-2、IL-4和抗-IFN-γ一起培养。进行流式细胞术、实时定量 PCR (qRT-PCR) 和 ELISA 以检测 T 辅助 9 (Th9) 细胞、IL-9 表达和 IL-9 释放。进行蛋白质印迹以检查磷酸化 (p)-IKKα、p-IκBα、p-p65 和 IRF4 水平。采用苏木精/伊红（H&E）染色评估肺组织病理变化。抑制 Sgk1 可显着逆转哮喘小鼠肺组织中升高的 Th9 细胞和 IL-9 表达。在体外，Sgk1 促进 Th9 分化并提高 p-IKKα、p-IκBα、p-p65 和 IRF4 水平，但是抑制 IKKα/IκBα/p65 通路和 IRF4 都可以逆转 Sgk1 增强的 Th9 分化。Sgk1→IKKα/IκBα/NF-κBp65→IRF4→Th9 轴可能与哮喘发展有关。