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首页> 外文期刊>Infection and immunity >In Vivo Regulation of the Vi Antigen in Salmonella and Induction of Immune Responses with an In Vivo-Inducible Promoter
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In Vivo Regulation of the Vi Antigen in Salmonella and Induction of Immune Responses with an In Vivo-Inducible Promoter

机译：沙门氏菌体内抗原的体内调节和体内诱导型启动子的免疫应答诱导。

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摘要

Salmonella enterica serovar Typhi, the agent of typhoid fever in humans, expresses the surface Vi polysaccharide antigen that contributes to virulence. However, Vi expression can also be detrimental to some key steps of S. Typhi infectivity, for example, invasion, and Vi is the target of protective immune responses. We used a strain of S. Typhimurium carrying the whole Salmonella pathogenicity island 7 (SPI-7) to monitor in vivo Vi expression within phagocytic cells of mice at different times after systemic infection. We also tested whether it is possible to modulate Vi expression via the use of in vivo-inducible promoters and whether this would trigger anti-Vi antibodies through the use of Vi-expressing live bacteria. Our results show that Vi expression in the liver and spleen is downregulated with the progression of infection and that the Vi-negative population of bacteria becomes prevalent by day 4 postinfection. Furthermore, we showed that replacing the natural tviA promoter with the promoter of the SPI-2 gene ssaG resulted in sustained Vi expression in the tissues. Intravenous or oral infection of mice with a strain of S. Typhimurium expressing Vi under the control of the ssaG promoter triggered detectable levels of all IgG subclasses specific for Vi. Our work highlights that Vi is downregulated in vivo and provides proof of principle that it is possible to generate a live attenuated vaccine that induces Vi-specific antibodies after single oral administration.
机译：肠伤寒沙门氏菌（Salmonella enterica serovar Typhi）是人类伤寒的一种病原，它表达有助于毒力的表面六价多糖抗原。但是，Vi的表达也可能损害 S 的某些关键步骤。Typhi的感染性，例如入侵，Vi是保护性免疫反应的目标。我们使用携带整个沙门氏菌致病岛7（SPI-7）的 S。鼠伤寒菌株来监测小鼠全身吞噬后不同时间吞噬细胞内的体内 Vi表达感染。我们还测试了是否有可能通过使用体内诱导型启动子来调节Vi的表达，以及是否通过使用表达Vi的活细菌来触发抗Vi抗体。我们的结果表明，肝脏和脾脏中的Vi表达随着感染的进行而下调，并且感染后第4天，细菌的Vi阴性菌群变得普遍。此外，我们发现用SPI-2基因 ssaG 的启动子替换天然的 tviA 启动子会导致组织中持续的Vi表达。在 ssaG 启动子的控制下，表达Vi的 S。鼠伤寒毒株的小鼠的静脉或口服感染触发了可检测到的所有Vi特异性IgG亚类水平。我们的工作强调Vi在体内被下调，并提供了原理证明，即单次口服给药后，可能会产生减毒活疫苗，诱导Vi特异性抗体。

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