Borrelia burgdorferi bba66 gene inactivation results in attenuated mouse infection by tick transmission.

Borrelia burgdorferi bba66 gene inactivation results in attenuated mouse infection by tick transmission.
复制标题

伯氏疏螺旋体 bba66 基因失活导致蜱传播引起的小鼠感染减弱。

DOI:
10.1128/iai.00140-13
复制
发表时间:
2013
影响因子:
3.1
通讯作者:
Gilmore,RobertD
Gilmore,RobertD
中科院分区:
医学2区
文献类型:
--
作者:
Patton,ToniG;Brandt,KevinS;Nolder,Christi;Clifton,DawnR;Carroll,JamesA;Gilmore,RobertD

文献摘要

相似文献

通过灭活编码基因bba 66和表征整个自然小鼠-蜱-小鼠周期中的突变表型,评价了伯氏疏螺旋体表面定位的免疫原性脂蛋白BBA 66对载体和宿主感染的影响。BBA 66缺陷型突变分离株BbΔA66通过针头接种培养微生物在小鼠中保持感染性,但相对于亲本野生型(WT)菌株,观察到胫跗关节中螺旋体负荷和病理学差异。肩突硬蜱幼虫取食感染小鼠后成功获得BbΔ A66,并在这些蜱中持续存在直至蜕皮。一系列的蜱传播实验(n= 7)表明,BbΔA66感染的蜱感染实验室小鼠的能力与WT感染的蜱喂养的小鼠相比显著受损。BbΔ A66与完整拷贝的bba 66的反式互补通过蜱传播恢复了小鼠的WT感染表型。这些结果表明BBA 66在促进B中的作用。作为莱姆病疏螺旋体病的疾病过程的一部分,从蜱媒介到哺乳动物宿主的伯氏疏螺旋体传播和传播。
The impact of the Borrelia burgdorferi surface-localized immunogenic lipoprotein BBA66 on vector and host infection was evaluated by inactivating the encoding gene,bba66, and characterizing the mutant phenotype throughout the natural mouse-tick-mouse cycle. The BBA66-deficient mutant isolate, BbΔA66, remained infectious in mice by needle inoculation of cultured organisms, but differences in spirochete burden and pathology in the tibiotarsal joint were observed relative to the parental wild-type (WT) strain. Ixodes scapularis larvae successfully acquired BbΔA66following feeding on infected mice, and the organisms persisted in these ticks through the molt to nymphs. A series of tick transmission experiments (n= 7) demonstrated that the ability of BbΔA66-infected nymphs to infect laboratory mice was significantly impaired compared to that of mice fed upon by WT-infected ticks.trans-complementation of BbΔA66with an intact copy ofbba66restored the WT infectious phenotype in mice via tick transmission. These results suggest a role for BBA66 in facilitating B. burgdorferi dissemination and transmission from the tick vector to the mammalian host as part of the disease process for Lyme borreliosis.