Deletion of BBA64, BBA65, and BBA66 loci does not alter the infectivity of Borrelia burgdorferi in the murine model of Lyme disease.
Deletion of BBA64, BBA65, and BBA66 loci does not alter the infectivity of Borrelia burgdorferi in the murine model of Lyme disease.
复制标题
BBA64、BBA65 和 BBA66 位点的删除不会改变莱姆病小鼠模型中伯氏疏螺旋体的感染性。
DOI：
10.1128/iai.00803-08
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发表时间：
2008
影响因子：
3.1
通讯作者：
Seshu,J
中科院分区：
文献类型：
--
作者：
Maruskova,Mahulena;Seshu,J
莱姆病的病原体伯氏疏螺旋体改变其基因表达，以响应其蜱虫载体与脊椎动物宿主中遇到的高度不同的环境信号。全基因组转录谱分析。在大肠杆菌宿主特异性条件下体外繁殖的burgdorferi，揭示了几个线性质粒54（lp 54）编码的开放阅读框（ORF）的显著上调。在这些ORF中，BBA 64、BBA 65和BBA 66已被证明响应于多种拟南芥宿主特异性信号而上调。最近，我们确定BBA 64 −突变体感染C3 H/HeN小鼠的能力与其同基因对照菌株相比没有显著差异，表明B. burgdorf可能利用多种功能相关的决定因素来建立感染。我们进一步在B的非感染性lp 25 −克隆分离物中产生了BBA 65 −和BBA 66 −单一突变体。并用恢复感染性所需的lp 25的最小区域（BBE 22）补充它们。此外，我们使用B的感染性克隆分离物产生了BBA 64 − BBA 65 − BBA 66 −三重突变体。具有所有感染相关质粒的伯氏菌株B31（5A 11）。在感染后第21天和第62天，与其各自的同基因亲本菌株相比，通过皮内针接种用单个突变体或三重突变体感染的C3 H/HeN小鼠的不同组织分离活螺旋体的能力没有显著差异。这些观察表明B.在莱姆病的鼠模型中，在BBA 64、BBA 65和BBA 66不表达的情况下，burgdorferican建立感染。
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 ofB. 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 thatB. burgdorferimight utilize multiple, functionally related determinants to establish infection. We further generated BBA65−and BBA66−single mutants in a noninfectious, lp25−clonal isolate ofB. burgdorferistrain 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 ofB. burgdorferistrain 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 thatB. burgdorferican establish infection in the absence of expression of BBA64, BBA65, and BBA66 in the murine model of Lyme disease.