研究动态
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经过呼吸机相关性肺炎(ventilator associated pneumonia,VAP)后,通过调节AKT3/GXP4,巨噬细胞的耗竭减轻了肺损伤。

Macrophages depletion alleviates lung injury by modulating AKT3/GXP4 following ventilator associated pneumonia.

发表日期:2023
作者: Youfeng Zhu, Yang Chen, Di Xie, Dong Xia, Huanming Kuang, Xinmin Guo, Bo Ning
来源: Frontiers in Immunology

摘要:

AKT3 在肺癌中似乎扮演着一定的角色。然而,它在呼吸机相关性肺炎中的作用尚不清楚。因此,本研究旨在调查呼吸机相关性肺炎中AKT3在巨噬细胞中的作用。AKT3的mRNA水平来自癌症基因组图谱(TCGA)、基因表达数据库(GEO),并使用仙桃学术分析工具进行数据分析。此外,在体实验探究了AKT3在呼吸机相关性肺炎(VAP)中的作用。AKT3在不同正常和肿瘤组织中表达差异明显。功能富集分析显示AKT3在肺癌中具有免疫调节功能和炎症反应。巨噬细胞的消耗保护了肺上皮细胞,并显著降低了MMP9、MMP19、FTH和FTL表达水平,并增加了GPX4表达水平,同时部分逆转了巨噬细胞的变化。机制上,巨噬细胞消耗通过调节VAP后的AKT3减轻了肺上皮细胞的铁死亡。总的来说,本研究暗示了对AKT3在肺癌中的免疫调节功能需要进一步验证。此外,巨噬细胞的消耗通过调节AKT3/GPX4途径来缓解呼吸机相关性肺损伤。版权所有 © 2023 朱、陈、谢、夏、邝、郭和宁。
AKT3 appears to play a role in lung cancer. However, its role in ventilator-associated pneumonia is still unclear. Therefore, this study aimed to investigate the role of AKT3 in macrophages during ventilator-associated pneumonia.The mRNA level of AKT3, Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), The data is analyzed using the Xiantao academic analysis tool. Additionally, the roles of AKT3 in ventilator-associated pneumonia (VAP) were investigated through in vivo experiments.AKT3 was differentially expressed in various normal and tumor tissues. Functional enrichment analysis indicated the immunomodulatory function and inflammatory response of AKT3 in lung cancer. Depletion of macrophages protected against lung epithelial cells and significantly decreased MMP9, MMP19, FTH, and FTL expression levels and increased GPX4 expression levels, while partially reversing the changes in macrophage. Mechanistically, macrophage depletion attenuates ferroptosis of lung epithelial cells by modulating AKT3 following VAP.Collectively, this study suggests the need for further validation of the immunoregulatory function of AKT3 in lung cancer. Additionally, macrophage depletion mitigates lung injury by modulating the AKT3/GPX4 pathway in the context of VAP.Copyright © 2023 Zhu, Chen, Xie, Xia, Kuang, Guo and Ning.