Clinical Unit of Infectious Diseases, Microbiology, and Preventive Medicine, Institute of Biomedicine of Seville, University Hospital Virgen del Rocío, Consejo Superior de Investigaciones Científicas, University of Seville, Seville, Spain.
Department of Medicine, University of Seville, Seville, Spain.
J Infect Dis. 2020 Sep 1;222(7):1204-1212. doi: 10.1093/infdis/jiaa201.
Acinetobacter baumannii is a successful pathogen responsible for infections with high mortality rate. During the course of infection it can be found in microaerobic environments, which influences virulence factor expression. From a previous transcriptomic analysis of A. baumannii ATCC 17978 under microaerobiosis, we know the gene pstS is overexpressed under microaerobiosis. Here, we studied its role in A. baumannii virulence. pstS loss significantly decreased bacterial adherence and invasion into A549 cells and increased A549 cell viability. pstS loss also reduced motility and biofilm-forming ability of A. baumannii. In a peritoneal sepsis murine model, the minimum lethal dose required by A. baumannii ATCC 17978 ΔpstS was lower compared to the wild type (4.3 vs 3.2 log colony forming units/mL, respectively), and the bacterial burden in tissues and fluids was lower. Thus, the loss of the phosphate sensor PstS produced a decrease in A. baumannii pathogenesis, supporting its role as a virulence factor.
鲍曼不动杆菌是一种成功的病原体，可导致高死亡率的感染。在感染过程中，它可以在微需氧环境中被发现，这会影响毒力因子的表达。在先前对鲍曼不动杆菌 ATCC 17978 在微需氧条件下的转录组分析中，我们知道 pstS 基因在微需氧条件下过度表达。在这里，我们研究了它在鲍曼不动杆菌毒力中的作用。pstS 缺失显著降低了细菌对 A549 细胞的黏附和侵袭，并增加了 A549 细胞的活力。pstS 缺失还降低了鲍曼不动杆菌的运动性和生物膜形成能力。在腹膜炎脓毒症小鼠模型中，与野生型相比，鲍曼不动杆菌 ATCC 17978 ΔpstS 所需的最小致死剂量降低（分别为 4.3 和 3.2 log 菌落形成单位/mL），组织和液体中的细菌负荷也降低。因此，磷酸盐传感器 PstS 的缺失导致鲍曼不动杆菌发病机制下降，支持其作为毒力因子的作用。
