Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Curr Opin Rheumatol. 2010 Jul;22(4):451-5. doi: 10.1097/BOR.0b013e328338f73f.
Borrelia burgdorferi colonization of the joints induces an inflammatory response, which in some individuals progresses to chronic arthritis. In this review, we discuss novel pathways that are implicated in disease development by modulating host defenses to B. burgdorferi infection.
The use of transgenic mice and gene expression analyses has revealed novel pathways involved in pathogenesis of Lyme disease. It is now clear that B. burgdorferi exploits an array of salivary gland proteins of the tick to evade immune responses in the mammalian host. The spirochete also modulates its surface protein profile upon infection and induces anti-inflammatory cytokines, favoring survival of the pathogen. The host defense involves toll-like receptors (TLRs), such as TLR2 and others, in B. burgdorferi recognition. To further dissect the genetic predisposition to treatment-refractory Lyme arthritis, HLA-DR transgenic mice have been used.
The cause and pathogenesis of Lyme arthritis are complex. Elucidating the mechanisms that govern this chronic inflammatory response will provide direct insights into other infectious arthritides and the development of novel therapeutic approaches against B. burgdorferi infection.
伯氏疏螺旋体在关节中的定植会引起炎症反应，而在某些个体中，这种炎症反应会发展为慢性关节炎。在这篇综述中，我们讨论了通过调节宿主对伯氏疏螺旋体感染的防御，参与疾病发展的新途径。
利用转基因小鼠和基因表达分析，揭示了与莱姆病发病机制相关的新途径。现在很清楚，伯氏疏螺旋体利用蜱的一系列唾液腺蛋白来逃避哺乳动物宿主的免疫反应。螺旋体在感染时还会调节其表面蛋白谱，并诱导抗炎细胞因子，有利于病原体的存活。宿主防御涉及 TLR2 等 Toll 样受体（TLRs）对伯氏疏螺旋体的识别。为了进一步剖析治疗抵抗性莱姆关节炎的遗传易感性，已经使用了 HLA-DR 转基因小鼠。
莱姆关节炎的病因和发病机制很复杂。阐明控制这种慢性炎症反应的机制将为其他感染性关节炎的发病机制和针对伯氏疏螺旋体感染的新型治疗方法的开发提供直接的见解。
