BBA52 facilitates Borrelia burgdorferi transmission from feeding ticks to murine hosts.

BBA52 facilitates Borrelia burgdorferi transmission from feeding ticks to murine hosts.
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DOI:
10.1086/651172
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发表时间:
2010-04-01
期刊:
The Journal of infectious diseases
影响因子:
--
通讯作者:
Pal U
Pal U
中科院分区:
其他
文献类型:
--
作者:
Kumar M;Yang X;Coleman AS;Pal U

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莱姆病的病原体伯氏疏螺旋体通过蜱-啮齿动物传播周期在自然界中持续存在。对微生物转录组的选择性评估(仅限于编码推定膜蛋白的基因)显示,bba 52在体内的转录严格限于微生物生命周期的载体特异性部分,在喂食蜱中表达水平最高,在小鼠中表达迅速下调。如通过关节炎和心脏炎的发生或小鼠或蜱中的长期病原体持续性所评估的,BBA 52缺失不影响鼠疾病。然而,bba 52缺陷确实会损害宿主和载体之间的微生物转换,当bba 52表达在基因上恢复到原始基因组位点时,这种缺陷可以得到完全挽救。这些研究证实BBA 52促进病原体的载体-宿主转换,因此是干扰B的潜在抗原靶标。从蜱到哺乳动物宿主的伯氏螺旋体传播。
Borrelia burgdorferi, the pathogen of Lyme borreliosis, persists in nature through a tick-rodent transmission cycle. A selective assessment of the microbial transcriptome, limited to gene encoding putative membrane proteins, reveals that bba52 transcription in vivo is strictly confined to the vector-specific portion of microbial life cycle with highest expression levels in feeding ticks and swift downregulation in mice. bba52 deletion did not affect murine disease as assessed by the genesis of arthritis and carditis or long-term pathogen persistence in mice or ticks. However, bba52 deficiency did impair microbial transitions between hosts and vector, defects that could be fully rescued when bba52 expression was genetically restored to the original genomic locus. These studies establish that BBA52 facilitates vector-host transitions by the pathogen and as such, is a potential antigenic target for interference with B. burgdorferi transmission from ticks to mammalian hosts.
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