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首页> 外文期刊>Infection and immunity >Deletion of BBA64, BBA65, and BBA66 Loci Does Not Alter the Infectivity of Borrelia burgdorferi in the Murine Model of Lyme Disease
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Deletion of BBA64, BBA65, and BBA66 Loci Does Not Alter the Infectivity of Borrelia burgdorferi in the Murine Model of Lyme Disease

机译：在莱姆病小鼠模型中，BBA64，BBA65和BBA66基因座的删除不会改变伯氏疏螺旋体的感染性

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Borrelia burgdorferi, the causative agent of Lyme disease, alters its gene expression in response to highly disparate environmental signals encountered in its tick vector versus vertebrate hosts. Whole-genome transcriptional profile analysis of B. burgdorferi, propagated in vitro under mammalian-host-specific conditions, revealed significant upregulation of several linear plasmid 54 (lp54)-encoded open reading frames (ORFs). Among these ORFs, BBA64, BBA65, and BBA66 have been shown to be upregulated in response to multiple mammalian-host-specific signals. Recently, we determined that there was no significant difference in the ability of BBA64? mutant to infect C3H/HeN mice compared to its isogenic control strains, suggesting that B. burgdorferi might utilize multiple, functionally related determinants to establish infection. We further generated BBA65? and BBA66? single mutants in a noninfectious, lp25? clonal isolate of B. burgdorferi strain B31 (ML23) and complemented them with the minimal region of lp25 (BBE22) required for restoring the infectivity. In addition, we generated a BBA64? BBA65? BBA66? triple mutant using an infectious, clonal isolate of B. burgdorferi strain B31 (5A11) that has all of the infection-associated plasmids. There were no significant differences in the ability to isolate viable spirochetes from different tissues of C3H/HeN mice infected via intradermal needle inoculation with either the individual single mutants or the triple mutant compared to their respective isogenic parental strains at days 21 and 62 postinfection. These observations suggest that B. burgdorferi can establish infection in the absence of expression of BBA64, BBA65, and BBA66 in the murine model of Lyme disease.
机译：莱姆病的致病菌 Borrelia burgdorferi 会响应壁虱载体与脊椎动物宿主中遇到的高度不同的环境信号而改变其基因表达。 B的全基因组转录谱分析。在哺乳动物宿主特异性条件下体外繁殖的burgdorferi 揭示了几个线性质粒54（lp54）编码的开放阅读框（ORF）的显着上调。在这些ORF中，已显示BBA64，BBA65和BBA66响应多种哺乳动物宿主特异性信号而被上调。最近，我们确定BBA64 ？突变体与其同基因对照菌株相比感染C3H / HeN小鼠的能力没有显着差异，表明 B。 burgdorferi 可能利用多个与功能相关的决定因素来确定感染。我们在非感染性 B的lp25 ？克隆分离物中进一步产生了BBA65 ？和BBA66 ？单个突变体。 burgdorferi菌株B31（ML23），并用恢复感染力所需的lp25最小区域（BBE22）对其进行了补充。另外，我们使用感染性克隆 B分离了BBA64 ？ BBA65 ？ BBA66 ？三重突变体。具有所有感染相关质粒的burgdorferi菌株B31（5A11）。与在感染后第21天和第62天相比，分别用单个单突变体或三重突变体通过皮内注射接种的C3H / HeN小鼠感染的不同组织分离活体螺旋体的能力与它们各自的同基因亲本菌株相比没有显着差异。这些发现表明 B。 burgdorferi 可以在莱姆病鼠模型中不存在BBA64，BBA65和BBA66表达的情况下建立感染。

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