Lederer Sharon, Brenner Christiane, Stehle Thomas, Gern Lise, Wallich Reinhard, Simon Markus M
Max-Planck-Institut für Immunobiologie, Freiburg, Germany.
Med Microbiol Immunol. 2005 Jan;194(1-2):81-90. doi: 10.1007/s00430-004-0218-1.
Adaptation of Borrelia burgdorferi in the vector and vertebrate host is mediated by mechanisms that regulate differential expression of outer surface lipoproteins (Osps). In this study, real time PCR was applied to quantify tissue-specific expression of four linear plasmid (lp54)-encoded (ospA, zs7.a36, zs7.a66 zs7.a68) and one circular plasmid (cp26)-encoded (ospC) gene from B. burgdorferi sensu stricto, in a natural setting of tick-infected immunodeficient (C.B-17 SCID) and immunocompetent (BALB/c and AKR/OlaHsd) mice for up to 120 days post-infection (p.i.). Early during infection (day 30 p.i.) high numbers of spirochetes were found in the heart and joint, but not the ear and spleen tissues of disease-susceptible SCID mice. In disease-susceptible AKR mice spirochetes colonized the ear and joint tissues, but were undetectable in tissues of disease-resistant BALB/c mice. Later in infection (day 120 p.i.), spirochetes had expanded (approximately 1,000-fold) in all SCID tissues tested but were undetectable in AKR and BALB/c mice. Of the five genes analyzed, only zs7.a36 transcripts were detected in various tissues of all infected mouse strains, though at differing levels, whereas ospC transcripts were only found in tissue specimens of SCID mice. Furthermore, gene expression of ospC and zs7.a36 appears to be differentially regulated in distinct organs of individual mice. In contrast, transcripts for ospA, zs7.a66, and zs7.a68 were not detected in any of the mouse strains, independent of their immune status and/or the severity of their infection/inflammatory responses. Late during infection (day 120 p.i.), transcription of zs7.a36 and ospC was down-regulated in the tissues of SCID mice despite expansion of spirochetes. This type of quantitative analysis may be helpful to further disclose principles of pathogenesis of Lyme borreliosis and to design strategies for its therapeutic treatment.
伯氏疏螺旋体在媒介和脊椎动物宿主中的适应性是由调节外表面脂蛋白（Osps）差异表达的机制介导的。在本研究中，应用实时PCR定量分析了来自严格意义上的伯氏疏螺旋体的四个线性质粒（lp54）编码基因（ospA、zs7.a36、zs7.a66、zs7.a68）和一个环状质粒（cp26）编码基因（ospC）在蜱感染的免疫缺陷（C.B-17 SCID）和免疫 competent（BALB/c和AKR/OlaHsd）小鼠自然环境中的组织特异性表达，感染后（p.i.）长达120天。在感染早期（感染后第30天），在易感SCID小鼠的心脏和关节中发现大量螺旋体，但在耳朵和脾脏组织中未发现。在易感AKR小鼠中，螺旋体定殖于耳朵和关节组织，但在抗病BALB/c小鼠的组织中未检测到。在感染后期（感染后第120天），螺旋体在所有测试的SCID组织中数量增加（约1000倍），但在AKR和BALB/c小鼠中未检测到。在分析的五个基因中，只有zs7.a36转录本在所有感染小鼠品系的各种组织中被检测到，尽管水平不同，而ospC转录本仅在SCID小鼠的组织标本中发现。此外，ospC和zs7.a36的基因表达在个体小鼠的不同器官中似乎受到不同调节。相比之下，ospA、zs7.a66和zs7.a68的转录本在任何小鼠品系中均未检测到，与它们的免疫状态和/或感染/炎症反应的严重程度无关。在感染后期（感染后第120天），尽管螺旋体数量增加，但SCID小鼠组织中zs7.a36和ospC的转录被下调。这种定量分析可能有助于进一步揭示莱姆病的发病机制原理，并设计其治疗策略。
