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首页> 美国卫生研究院文献>NPJ Vaccines >Immunisation of two rodent species with new live-attenuated mutants of Yersinia pestis CO92 induces protective long-term humoral- and cell-mediated immunity against pneumonic plague
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Immunisation of two rodent species with new live-attenuated mutants of Yersinia pestis CO92 induces protective long-term humoral- and cell-mediated immunity against pneumonic plague

机译：用鼠疫耶尔森菌新的减毒活体突变体对两个啮齿动物进行免疫可诱导其对肺鼠疫的长期体液免疫和细胞介导的免疫保护

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We showed recently that the live-attenuated Δlpp ΔmsbB Δail and Δlpp ΔmsbB::ailL2 mutants of Yersinia pestis CO92 provided short-term protection to mice against developing subsequent lethal pneumonic plague. These mutants were either deleted for genes encoding Braun lipoprotein (Lpp), an acetyltransferase (MsbB) and the attachment invasion locus (Ail) (Δlpp ΔmsbB Δail) or contained a modified version of the ail gene with diminished virulence (Δlpp ΔmsbB::ailL2). Here, long-term immune responses were first examined after intramuscular immunisation of mice with the above-mentioned mutants, as well as the newly constructed Δlpp ΔmsbB Δpla mutant, deleted for the plasminogen-activator protease (pla) gene instead of ail. Y. pestis-specific IgG levels peaked between day 35 and 56 in the mutant-immunised mice and were sustained until the last tested day 112. Splenic memory B cells peaked earlier (day 42) before declining in the Δlpp ΔmsbB::ailL2 mutant-immunised mice while being sustained for 63 days in the Δlpp ΔmsbB Δail and Δlpp ΔmsbB Δpla mutant-immunised mice. Splenic CD4+ T cells increased in all immunised mice by day 42 with differential cytokine production among the immunised groups. On day 120, immunised mice were exposed intranasally to wild-type (WT) CO92, and 80–100% survived pneumonic challenge. Mice immunised with the above-mentioned three mutants had increased innate as well as CD4+ responses immediately after WT CO92 exposure, and coupled with sustained antibody production, indicated the role of both arms of the immune response in protection. Likewise, rats vaccinated with either Δlpp ΔmsbB Δail or the Δlpp ΔmsbB Δpla mutant also developed long-term humoral and cell-mediated immune responses to provide 100% protection against developing pneumonic plague. On the basis of the attenuated phenotype, the Δlpp ΔmsbB Δail mutant was recently excluded from the Centers for Disease Control and Prevention select agent list.
机译：最近，我们显示了鼠疫耶尔森菌CO92的活减毒ΔlppΔmsbBΔail和ΔlppΔmsbB:: ailL2突变体为小鼠提供了短期保护，使其免受随后的致命性肺炎鼠疫的侵害。这些突变体要么缺失编码Braun脂蛋白（Lpp），乙酰基转移酶（MsbB）和附着侵袭位点（Ail）（ΔlppΔmsbBΔail）的基因，要么包含具有弱毒力的ail基因的修饰版本（ΔlppΔmsbB:: ailL2 ）。在这里，在对上述突变体以及新构建的ΔlppΔmsbBΔpla突变体进行肌肉免疫小鼠后，首先检查了长期免疫应答，删除了纤溶酶原激活物蛋白酶（pla）基因而不是 ail基因。是的突变的-免疫小鼠的鼠疫特异性IgG水平在第35至56天达到峰值，并持续到最后测试的第112天。脾脏记忆B细胞在下降之前更早达到峰值（第42天）在Δ lpp Δ msbB :: ailL2 突变免疫小鼠中，同时在Δ lpp Δ msbB < / em>Δ ail 和Δ lpp Δ msbB Δ pla 免疫突变的小鼠。到第42天，所有免疫小鼠的脾CD4 + T细胞均增加，免疫组间细胞因子产生差异。在第120天，经免疫的小鼠经鼻腔内暴露于野生型（WT）CO92，80-100％的肺炎攻击存活下来。用上述三种突变体免疫的小鼠在WT CO92暴露后立即具有先天性以及CD4 + 应答增加，并伴随持续的抗体产生，表明免疫应答的两臂在保护中的作用。同样，用Δ lpp Δ msbB Δ ail 或Δ lpp Δ msbB < / em>Δ pla 突变体还开发了长期的体液和细胞介导的免疫反应，以提供100％的保护，以预防肺炎性鼠疫的发展。根据减毒表型，最近从疾病控制和预防中心选择剂中排除了Δ lpp Δ msbB Δ ail 突变体清单。

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