Acinetobacter baumannii is a ubiquitous Gram-negative bacterium, that is associated with significant disease in immunocompromised individuals. The success of A. baumannii is partly attributable to its high level of antibiotic resistance. Further, A. baumannii expresses a broad arsenal of putative zinc efflux systems that are likely to aid environmental persistence and host colonization, but detailed insights into how the bacterium deals with toxic concentrations of zinc are lacking. In this study we present the transcriptomic responses of A. baumannii to toxic zinc concentrations. Subsequent mutant analyses revealed a primary role for the resistance-nodulation-cell division heavy metal efflux system CzcCBA, and the cation diffusion facilitator transporter CzcD in zinc resistance. To examine the role of zinc at the host-pathogen interface we utilized a murine model of zinc deficiency and challenge with wild-type and czcA mutant strains, which identified highly site-specific roles for zinc during A. baumannii infection. Overall, we provide novel insight into the key zinc resistance mechanisms of A. baumannii and outline the role these systems play in enabling the bacterium to survive in diverse environments.

中文翻译：

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锌外排在鲍曼不动杆菌感染中的作用。

鲍曼不动杆菌是一种普遍存在的革兰氏阴性细菌，与免疫功能低下的个体中的重大疾病有关。鲍曼不动杆菌的成功部分归因于其高水平的抗生素抗性。此外，鲍曼不动杆菌表达了广泛的假定的锌外排系统，该系统可能有助于环境持久性和宿主定殖，但是缺乏关于细菌如何处理锌的毒性浓度的详细见解。在这项研究中，我们介绍了鲍曼不动杆菌对有毒锌浓度的转录组学反应。随后的突变分析表明，电阻-结节-细胞分裂重金属外排系统CzcCBA和阳离子扩散促进剂转运体CzcD在锌抗性中起主要作用。为了检查锌在宿主-病原体界面上的作用，我们利用了锌缺乏和野生型和czcA突变株攻击的鼠模型，该突变株确定了鲍曼不动杆菌感染期间锌的高度位点特异性作用。总的来说，我们对鲍曼不动杆菌的关键锌抗性机制提供了新颖的见解，并概述了这些系统在使细菌能够在多种环境中存活的作用。