Abstract

Acinetobacter baumannii has become a leading cause of bacterial nosocomial infections, in part, due to its ability to resist desiccation, disinfection and antibiotics. Several factors contribute to the tenacity and virulence of this pathogen, including production of a broad range of surface glycoconjugates, secretory systems and efflux pumps. We became interested in examining the importance of trehalose in A. baumannii after comparing intact bacterial cells by high-resolution magic angle spinning nuclear magnetic resonance and by noting high levels of this disaccharide, obscuring all other resonances in the spectrum. Since this was observed under normal growth conditions, we speculated that trehalose must serve additional functions beyond osmolyte homeostasis. Using the virulent isolate A. baumannii AB5075 and mutants in the trehalose synthesis pathway, osmoregulatory trehalose synthesis proteins A and B (△otsA and △otsB), we found that the trehalose-deficient △otsA showed increased sensitivity to desiccation, colistin, serum complement and peripheral blood mononuclear cells, while trehalose-6-phosphate producing △otsB behaved similar to the wild-type. The △otsA mutant also demonstrated increased membrane permeability and loss of capsular polysaccharide. These findings demonstrate that trehalose deficiency leads to loss of virulence in A. baumannii AB5075.

中文翻译：

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海藻糖缺乏的鲍曼不动杆菌通过失去荚膜多糖和老化膜完整性表现出降低的毒力

摘要

鲍曼不动杆菌已成为细菌性医院感染的主要原因，部分原因在于其抗干燥、消毒和抗生素的能力。有几个因素促成了这种病原体的韧性和毒力，包括产生广泛的表面糖缀合物、分泌系统和外排泵。在通过高分辨率魔角旋转核磁共振比较完整的细菌细胞并注意到这种二糖的高水平，掩盖了光谱中的所有其他共振之后，我们开始有兴趣检查海藻糖在鲍曼不动杆菌中的重要性。由于这是在正常生长条件下观察到的，我们推测海藻糖必须在渗透压稳态之外提供额外的功能。使用毒性分离物A. baumannii AB5075 和海藻糖合成途径中的突变体，渗透压调节海藻糖合成蛋白 A 和 B（△ otsA和△otsB），我们发现海藻糖缺乏的 △ otsA对干燥、粘菌素、血清补体和外周血单核细胞的敏感性增加细胞，同时产生海藻糖-6-磷酸△ otsB的行为与野生型相似。△ otsA突变体还表现出增加的膜通透性和荚膜多糖的损失。这些发现表明海藻糖缺乏会导致鲍曼不动杆菌AB5075的毒力丧失。