外表面蛋白 C 是伯氏疏螺旋体在哺乳动物感染期间的传播促进因子。
Outer surface protein C is a dissemination-facilitating factor of Borrelia burgdorferi during mammalian infection.
机构信息
Department of Pathobiological Sciences, Louisiana State University, Baton Rouge, Louisiana, United States of America.
出版信息
PLoS One. 2010 Dec 31;5(12):e15830. doi: 10.1371/journal.pone.0015830.
BACKGROUND
The Lyme disease spirochete Borrelia burgdorferi dramatically upregulates outer surface protein C (OspC) in response to fresh bloodmeal during transmission from the tick vector to a mammal, and abundantly produces the antigen during early infection. As OspC is an effective immune target, to evade the immune system B. burgdorferi downregulates the antigen once the anti-OspC humoral response has developed, suggesting an important role for OspC during early infection.
METHODOLOGY/PRINCIPAL FINDINGS: In this study, a borrelial mutant producing an OspC antigen with a 5-amino-acid deletion was generated. The deletion didn't significantly increase the 50% infectious dose or reduce the tissue bacterial burden during infection of the murine host, indicating that the truncated OspC can effectively protect B. burgdorferi against innate elimination. However, the deletion greatly impaired the ability of B. burgdorferi to disseminate to remote tissues after inoculation into mice.
CONCLUSIONS/SIGNIFICANCE: The study indicates that OspC plays an important role in dissemination of B. burgdorferi during mammalian infection.
背景
在莱姆病螺旋体博氏疏螺旋体从蜱传播媒介到哺乳动物的传播过程中，新鲜血餐会显著上调外表面蛋白 C（OspC），并在早期感染期间大量产生抗原。由于 OspC 是一种有效的免疫靶标，因此博氏疏螺旋体一旦产生针对 OspC 的体液免疫反应，就会下调该抗原，这表明 OspC 在早期感染中具有重要作用。
方法/主要发现：在这项研究中，生成了一种产生 5 个氨基酸缺失的 OspC 抗原的博莱氏疏螺旋体突变体。该缺失并未显著增加 50%感染剂量，也未减少感染宿主的组织细菌负荷，表明截短的 OspC 可有效地保护博氏疏螺旋体免受先天消除。然而，该缺失极大地削弱了博氏疏螺旋体在接种到小鼠后向远处组织传播的能力。
结论/意义：该研究表明，OspC 在哺乳动物感染期间博氏疏螺旋体的传播中发挥重要作用。
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