Brucella Manipulates Host Cell Ferroptosis to Facilitate Its Intracellular Replication and Egress in RAW264.7 Macrophages
文献类型： 外文期刊
作者： Zhang, Guangdong 1 ; Hu, Hai 1 ; Yin, Yi 1 ; Tian, Mingxing 1 ; Bu, Zhigao 2 ; Ding, Chan 1 ; Yu, Shengqing 1 ;
作者机构： 1.Chinese Acad Agr Sci CAAS, Shanghai Vet Res Inst, Shanghai 200241, Peoples R China
2.Chinese Acad Agr Sci CAAS, Harbin Vet Res Inst, Harbin 150069, Peoples R China
3.Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Peoples R China
关键词： Brucella; ferroptosis; glutathione peroxidase 4 (GPX4); GTP cyclohydrolase1 (GCH1); intracellular replication; bacterial egress
期刊名称：ANTIOXIDANTS （ 影响因子：7.0； 五年影响因子：7.3 ）
ISSN：
年卷期： 2024 年 13 卷 5 期
页码：
收录情况： SCI
摘要： Brucella virulence relies on its successful intracellular life cycle. Modulating host cell death is a strategy for Brucella to survive and replicate intracellularly. Ferroptosis is a novel regulated cell death characterized by iron-triggered excessive lipid peroxidation, which has been proven to be associated with pathogenic bacteria infection. Thus, we attempted to explore if smooth-type Brucella infection triggers host cell ferroptosis and what role it plays in Brucella infection. We assessed the effects of Brucella infection on the lactate dehydrogenase release and lipid peroxidation levels of RAW264.7 macrophages; subsequently, we determined the effect of Brucella infection on the expressions of ferroptosis defense pathways. Furthermore, we determined the role of host cell ferroptosis in the intracellular replication and egress of Brucella. The results demonstrated that Brucella M5 could induce ferroptosis of macrophages by inhibiting the GPX4-GSH axis at the late stage of infection but mitigated ferroptosis by up-regulating the GCH1-BH4 axis at the early infection stage. Moreover, elevating host cell ferroptosis decreased Brucella intracellular survival and suppressing host cell ferroptosis increased Brucella intracellular replication and egress. Collectively, Brucella may manipulate host cell ferroptosis to facilitate its intracellular replication and egress, extending our knowledge about the underlying mechanism of how Brucella completes its intracellular life cycle.
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