Yang Xianggui, Yu Xuejing, Zhou Li, Wang Dan, Chen Weixian
Department of Laboratory Medicine, the Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, P.R. China.
Department of Laboratory Medicine, Clinical Medical College and the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, 610500, P.R. China.
BMC Microbiol. 2025 Jan 9;25(1):10. doi: 10.1186/s12866-024-03718-2.
Enterobacter cloacae is increasingly prevalent and resistant to multiple antibiotics, making it a significant pathogen in healthcare settings with high mortality rates. However, its pathogenic mechanisms are not fully understood.
In this study, we explored the role of nagZ in regulating the virulence of E. cloacae and its potential as a therapeutic target. Our research showed that pathogenic strains of E. cloacae express higher levels of nagZ than colonizing strains, particularly in simulated infection environments. Deleting nagZ significantly reduced E. cloacae virulence in various infection models, including Galleria mellonella larvae, mice, and RAW264.7 cells. Moreover, nagZ knockout decreased the bacterium's ability to induce inflammatory factor levels, while complementing nagZ in knockout strains partially rescued this ability. Importantly, the absence of nagZ also enhanced the antibacterial efficacy of ceftazidime against E. cloacae.
These findings underscore the crucial role of nagZ in E. cloacae pathogenesis and highlight its potential as a novel therapeutic target for treating infections caused by this pathogen.
阴沟肠杆菌日益普遍且对多种抗生素耐药，使其成为医疗环境中具有高死亡率的重要病原体。然而，其致病机制尚未完全明确。
在本研究中，我们探究了nagZ在调节阴沟肠杆菌毒力中的作用及其作为治疗靶点的潜力。我们的研究表明，阴沟肠杆菌的致病菌株比定植菌株表达更高水平的nagZ，尤其是在模拟感染环境中。删除nagZ显著降低了阴沟肠杆菌在多种感染模型中的毒力，包括大蜡螟幼虫、小鼠和RAW264.7细胞。此外，nagZ基因敲除降低了该细菌诱导炎症因子水平的能力，而在敲除菌株中补充nagZ可部分恢复此能力。重要的是，nagZ的缺失还增强了头孢他啶对阴沟肠杆菌的抗菌效果。
这些发现强调了nagZ在阴沟肠杆菌致病机制中的关键作用，并突出了其作为治疗该病原体所致感染的新型治疗靶点的潜力。
