Roles of Schlafen4 in acute pneumonia induced by inhalation infection of hypervirulent Klebsiella pneumoniae
10.7644/j.issn.1674-9960.2025.04.002
- VernacularTitle:Schlafen4在高毒力肺炎克雷伯菌吸入感染致小鼠急性肺炎中的作用
- Author:
Xiaoyu ZHU
1
;
Tongtong QIN
;
Jinhong ZHA
;
Dongsheng ZHOU
;
Wenhui YANG
;
Bo GAO
Author Information
1. 军事科学院军事医学研究院,北京 100071
- Keywords:
Schlafen4;
hypervirulent Klebsiella pneumoniae;
mice;
pneumonia;
neutrophil;
gene knockout
- From:
Military Medical Sciences
2025;49(4):250-256
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of Schlafen4(SLFN4)in acute pneumonia induced by hypervirulent Klebsiella pneumoniae(hvKp)via intratracheal aerosolization.Methods Differential expression gene Slfn4 was identified after infection with hvKp based on RNA sequencing(RNA-seq)and single-cell RNA sequencing(scRNA-seq)data before Slfn4-/-mice were obtained via CRISPR/Cas gene editing technology.Slfn4-/-mice and wild mice were challenged via intratracheal aerosolization.Mortality and weight changes were recorded for 14 d,while pathological changes and expression levels of interleukin-6(IL-6),IL-17A,IL-1β,and tumor necrosis factor-α(TNF-α)were detected at 48 h post-infection.Results SLFN4 expression was significantly increased in wild mice after infection with hvKp.Survival was significantly increased,and weight loss was mitigated before gradual recovery in Slfn4-/-mice after infection.The knockout of SLFN4 attenuated alveolar wall thickening,diminished neutrophil infiltration,and suppressed pro-inflammatory cytokine production(IL-6,IL-17A,IL-1β,TNF-α)in the lung at 48 h post-infection.Conclusion The deletion of SLFN4 may suppress the expression of specific pro-inflammatory cytokines and attenuate neutrophil over-recruitment in the lung,thereby alleviating pneumonia in mice after hvKp infection.
