The relationship of the lipoprotein SsaB, manganese and superoxide dismutase in Streptococcus sanguinis virulence for endocarditis.
The relationship of the lipoprotein SsaB, manganese and superoxide dismutase in Streptococcus sanguinis virulence for endocarditis.
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DOI：
10.1111/mmi.12625
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发表时间：
2014-06
影响因子：
3.6
通讯作者：
Kitten T
中科院分区：
文献类型：
--
作者：
Crump KE;Bainbridge B;Brusko S;Turner LS;Ge X;Stone V;Xu P;Kitten T
血链球菌定植于牙齿，是感染性心内膜炎的重要原因。我们先前的工作表明脂蛋白SsaB对S. sanguinis对心内膜炎的毒力，属于保守的金属转运蛋白LraI家族。在这项研究中，我们证明了ssaB突变体积累较少的锰和铁比它的父母。缺乏锰依赖性超氧化物歧化酶，SodA的突变体，是显着低于野生型在兔心内膜炎模型的毒性，但显着比ssaB突变体的毒性。ssaB和sodA突变都不影响对吞噬细胞杀伤的敏感性或心脏瓣膜定植的效率。所有菌株的动物毒力结果可以通过在生理水平的O2下在血清中生长细菌来重现。SodA活性降低，但没有消除ssaB突变体在血清和兔子。ssaB突变体在血清中的生长恢复后，添加Mn2+或去除O2。抗氧化剂补充实验表明，超氧阴离子和羟基自由基一起负责ssaB突变体的生长缺陷。我们的结论是锰的积累介导的SsaB运输系统赋予毒力，使细胞生长在氧气中，通过苏打依赖和独立的机制。
Streptococcus sanguinis colonizes teeth and is an important cause of infective endocarditis. Our prior work showed that the lipoprotein SsaB is critical for S. sanguinis virulence for endocarditis and belongs to the LraI family of conserved metal transporters. In this study, we demonstrated that an ssaB mutant accumulates less manganese and iron than its parent. A mutant lacking the manganese-dependent superoxide dismutase, SodA, was significantly less virulent than wild-type in a rabbit model of endocarditis, but significantly more virulent than the ssaB mutant. Neither the ssaB nor the sodA mutation affected sensitivity to phagocytic killing or efficiency of heart valve colonization. Animal virulence results for all strains could be reproduced by growing bacteria in serum under physiological levels of O2. SodA activity was reduced, but not eliminated in the ssaB mutant in serum and in rabbits. Growth of the ssaB mutant in serum was restored upon addition of Mn2+ or removal of O2. Antioxidant supplementation experiments suggested that superoxide and hydroxyl radicals were together responsible for the ssaB mutant’s growth defect. We conclude that manganese accumulation mediated by the SsaB transport system imparts virulence by enabling cell growth in oxygen through SodA-dependent and independent mechanisms.
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影响因子：
3.6
作者：
Anjem A;Varghese S;Imlay JA
通讯作者：
Imlay JA
影响因子：
3.2
作者：
ARCHIBALD, FS;FRIDOVICH, I
通讯作者：
FRIDOVICH, I
影响因子：
3.7
作者：
Chen YY;Shieh HR;Chang YC
通讯作者：
Chang YC
影响因子：
2.8
作者：
Chen, Lei;Ge, Xiuchun;Xu, Ping
通讯作者：
Xu, Ping
DOI：
10.1073/pnas.1203051109
发表时间：
2012-05-01
影响因子：
11.1
作者：
Barnese, Kevin;Gralla, Edith Butler;Cabelli, Diane E.
通讯作者：
Cabelli, Diane E.