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In vivo characterization of the psa genes from Streptococcus pneumoniae in multiple models of infection

机译:在多种型感染模型中来自链球菌肺炎链球菌的PSA基因的体内表征

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Differential fluorescence induction technology was used to identify promoters of Streptococcus pneumoniae genes that are expressed during lung infection of the mouse. Among the promoter clones that were identified multiple times was the psa promoter, which drives expression of the psaBCA operon. These genes have been identified previously and shown to encode a manganese permease system as well as play a role in the virulence of this organism. Mutations in psaB, psaC or psaA result in growth limitation in low manganese. The expression of the psa operon was examined in vivo and the virulence of deletion mutants of psaB, psaC, psaA and psaBCA was assessed in four different animal models of infection. The psa promoter was induced more than ten-fold in vivo using an intraperitoneal chamber implant model. The psaB, psaC and psaA mutants were completely attenuated in systemic, respiratory tract and otitis media infections. In addition, these mutants were unable to grow in an implanted peritoneal chamber, but growth was restored by the addition of manganese to the chambers.
机译:使用差分荧光感应技术鉴定肺炎链球菌基因的启动子,其在小鼠的肺部感染期间表达。在多次鉴定的启动子克隆中​​是PSA启动子,其推动PSABCA操纵子的表达。先前已经鉴定出这些基因并显示为编码锰氧气系统以及在该生物体的毒力中起作用。 PSAB,PSAC或PSAA中的突变导致低锰的生长局限性。在体内检查PSA操纵子的表达,并在四种不同的感染动物模型中评估了PSAB,PSAC,PSAA和PSABCA的缺失突变体的毒力。 PSA启动子使用腹腔室植入模型诱导体内超过十倍。 PSAB,PSAC和PSAA突变体在全身性,呼吸道和中耳炎感染中完全衰减。此外,这些突变体不能在植入的腹膜室中生长,但通过加入腔室加入锰的生长。

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