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首页> 外文期刊>Infection and immunity >Impact of the High-Affinity Proline Permease Gene (putP) on the Virulence of Staphylococcus aureus in Experimental Endocarditis
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Impact of the High-Affinity Proline Permease Gene (putP) on the Virulence of Staphylococcus aureus in Experimental Endocarditis

机译：高亲和力脯氨酸通透酶基因（putP）对实验性心内膜炎中金黄色葡萄球菌毒力的影响

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摘要

Staphylococcus aureus causes a wide variety of invasive human infections. However, delineation of the genes which are essential for the in vivo survival of this pathogen has not been accomplished to date. Using signature tag mutagenesis techniques and large mutant pool screens, previous investigators identified several major gene classes as candidate essential gene loci for in vivo survival; these include genes for amino acid transporters, oligopeptide transporters, and lantibiotic synthesis (W. R. Schwan, S. N. Coulter, E. Y. W. Ng, M. H. Langhorne, H. D. Ritchie, L. L. Brody, S. Westbrock-Wadman, A. S. Bayer, K. R. Folger, and C. K. Stover, Infect. Immun. 66:567–572, 1998). In this study, we directly compared the virulence of four such isogenic signature tag mutants with that of the parental strain (RN6390) by using a prototypical model of invasive S. aureus infection, experimental endocarditis (IE). The oligonucleotide signature tag (OST) mutant with insertional inactivation of the gene (putP) which encodes the high-affinity transporter for proline uptake exhibited significantly reduced virulence in the IE model across three challenge inocula (104 to 106 CFU) in terms of achievable intravegetation densities (P, <0.05). The negative impact of putP inactivation on in vivo survival in the IE model was confirmed by simultaneous challenge with the originalputP mutant and the parental strain as well as by challenge with a putP mutant in which this genetic inactivation was transduced into a distinct parental strain (S6C). In contrast, inactivation of loci encoding an oligopeptide transporter, a purine repressor, and lantibiotic biosynthesis had no substantial impact on the capacity of OST mutants to survive within IE vegetations. Thus, genes encoding the uptake of essential amino acids may well represent novel targets for new drug development. These data also confirm the utility of the OST technique as an important screening methodology for identifying candidate genes as requisite loci for the in vivo survival of S. aureus.
机译：金黄色葡萄球菌引起多种侵入性人类感染。然而，迄今为止，尚未完成对该病原体的体内存活必不可少的基因的描述。使用签名标签诱变技术和大型突变池筛选，以前的研究人员确定了几种主要的基因类别作为体内存活的候选必需基因位点。这些包括氨基酸转运蛋白，寡肽转运蛋白和羊毛硫抗生素合成的基因（WR Schwan，SN Coulter，EYW Ng，MH Langhorne，HD Ritchie，LL Brody，S.Westbrock-Wadman，AS Bayer，KR Folger和CK Stover，Infect Immun。66：567-572，1998）。在这项研究中，我们通过使用侵袭性 S的原型模型，直接比较了四个这样的等基因标记标签突变体与亲本菌株（RN6390）的毒性。金黄色葡萄球菌感染，实验性心内膜炎（IE）。编码高亲和力转运蛋白脯氨酸的基因（ putP ）插入失活的寡核苷酸签名标签（OST）突变体在IE模型中通过三个挑战接种物均显着降低了毒力（10 到10 6 CFU）可以达到的植被内密度（ P ，<0.05）。通过同时攻击原始的 putP 突变体和亲本菌株以及通过攻击 putP 灭活对IE模型体内存活的负面影响。 em> putP 突变体，其中这种遗传失活被转导为不同的亲本菌株（S6C）。相比之下，编码寡肽转运蛋白，嘌呤阻遏物和羊毛硫抗生素生物合成的基因座的失活对OST突变体在IE植被中生存的能力没有实质性影响。因此，编码摄取必需氨基酸的基因可能很好地代表了新药开发的新靶标。这些数据还证实了OST技术作为一种重要的筛选方法的实用性，该方法可用于鉴定候选基因作为em的体内存活的必要基因座。金黄色的。

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