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


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2023
Historique:
received: 18 07 2023
accepted: 14 08 2023
medline: 22 9 2023
pubmed: 21 9 2023
entrez: 21 9 2023
Statut: epublish

Résumé

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 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.

Sections du résumé

Background
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.
Methods
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
Results
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.
Conclusion
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.

Identifiants

pubmed: 37731502
doi: 10.3389/fimmu.2023.1260584
pmc: PMC10507695
doi:

Substances chimiques

AKT3 protein, human EC 2.7.11.1
Proto-Oncogene Proteins c-akt EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1260584

Informations de copyright

Copyright © 2023 Zhu, Chen, Xie, Xia, Kuang, Guo and Ning.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Youfeng Zhu (Y)

Department of Intensive Care Unit, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong, China.

Yang Chen (Y)

Department of Intensive Care Unit, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong, China.

Di Xie (D)

Department of Emergency, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Dong Xia (D)

Department of Intensive Care Unit, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong, China.

Huanming Kuang (H)

Department of Intensive Care Unit, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong, China.

Xinmin Guo (X)

Department of Ultrasonography, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong, China.

Bo Ning (B)

Department of Neurosurgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong, China.

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Classifications MeSH