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首页> 外文期刊>Infection and immunity >Deletion of a Cation Transporter Promotes Lysis in Streptococcus pneumoniae
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Deletion of a Cation Transporter Promotes Lysis in Streptococcus pneumoniae

机译：阳离子转运蛋白的删除促进肺炎链球菌的裂解

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Streptococcus pneumoniae is a significant human pathogen which causes respiratory and serious invasive diseases. Mg2+ is essential for life, and its concentration varies throughout the human body. Magnesium uptake plays an important role in the virulence of many bacterial pathogens. To study the Mg2+ uptake of S. pneumoniae strain D39, a mutant was generated in SPD1383, a P-type ATPase with homology to the Salmonella Mg2+ transporter MgtA, which has also been shown to be a Ca2+ exporter in strain TIGR4. Under low-Ca2+ conditions, mutation led to a growth defect in complex medium and the gene was nearly essential for growth under low-Mg2+ conditions. Addition of Mg2+ restored the normal growth of the mutant in all cases, but the addition of other divalent cations had no effect. Addition of Ca2+, Mn2+, and Zn2+ in the presence of high Mg2+ concentrations inhibited restoration of growth. The mutant was unable to proliferate in blood, which was also alleviated by the addition of Mg2+. The protein was located in the membrane and produced in various S. pneumoniae strains and pathogenic streptococcal species. Surprisingly, mutation of the gene led to an elevated toxicity for endothelial cells. This was caused by an increased amount of pneumolysin in the medium, mediated by elevated lysis of the mutant. Thus, in this study, we uncovered a role for SPD1383 in Mg2+ uptake and hypothesize that the protein is a Mg2+/Ca2+ antiporter. Furthermore, a disturbance in Mg2+ homeostasis seems to promote lysis of S. pneumoniae.
机译：肺炎链球菌是引起呼吸系统疾病和严重侵袭性疾病的重要人类病原体。 Mg2 +是生命必不可少的元素，其浓度在整个人体中各不相同。摄取镁在许多细菌病原体的毒力中起重要作用。为了研究肺炎链球菌D39菌株对Mg2 +的吸收，在SPD1383中产生了一个突变体，这是一种与沙门氏菌Mg2 +转运蛋白MgtA同源的P型ATP酶，该突变体还被证明是TIGR4株中的Ca2 +出口者。在低Ca2 +条件下，突变导致在复杂培养基中的生长缺陷，并且该基因对于在低Mg2 +条件下的生长几乎必不可少。在所有情况下，添加Mg2 +均可恢复突变体的正常生长，但添加其他二价阳离子则无效果。在高Mg2 +浓度下添加Ca2 +，Mn2 +和Zn2 +会抑制生长恢复。该突变体无法在血液中增殖，这也可以通过添加Mg2 +来缓解。该蛋白质位于膜中，并在各种肺炎链球菌菌株和病原性链球菌种中产生。出人意料的是，基因突变导致内皮细胞毒性增加。这是由于培养基中肺炎球菌溶血素的增加，而突变体裂解升高所介导的。因此，在这项研究中，我们发现了SPD1383在Mg2 +吸收中的作用，并假设该蛋白是Mg2 + / Ca2 +反向转运蛋白。此外，Mg2 +稳态的紊乱似乎会促进肺炎链球菌的溶解。

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