Fikrig E, Feng W, Barthold S W, Telford S R, Flavell R A
Section of Rheumatology, Department of Internal Medicine, Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA.
J Immunol. 2000 May 15;164(10):5344-51. doi: 10.4049/jimmunol.164.10.5344.
Antisera to BBK32 (a Borrelia burgdorferi fibronectin-binding protein) and BBK50, two Ags synthesized during infection, protect mice from experimental syringe-borne Lyme borreliosis. Therefore, B. burgdorferi bbk32 and bbk50 expression within Ixodes scapularis ticks and the murine host, and the effect of BBK32 and BBK50 antisera on spirochetes throughout the vector-host life cycle were investigated. bbk32 and bbk50 mRNA and protein were first detected within engorged ticks, demonstrating regulated expression within the vector. Then bbk32 expression increased in mice at the cutaneous site of inoculation. During disseminated murine infection, bbk32 and bbk50 were expressed in several murine tissues, and mRNA levels were greatest in the heart and spleen at 30 days. BBK32 antisera protected mice from tick-borne B. burgdorferi infection and spirochete numbers were reduced by 90% within nymphs that engorged on immunized mice. Moreover, 75% of these ticks did not retain spirochetes upon molting, and subsequent B. burgdorferi transmission by adult ticks was impaired. Larval acquisition of B. burgdorferi by I. scapularis was also inhibited by BBK32 antisera. These data demonstrate that bbk32 and bbk50 are expressed during tick engorgement and that BBK32 antisera can interfere with spirochete transmission at various stages of the vector-host life cycle. These studies provide insight into mechanisms of immunity to Lyme borreliosis and other vector-borne diseases.
针对BBK32（一种伯氏疏螺旋体纤连蛋白结合蛋白）和BBK50（感染期间合成的两种抗原）的抗血清可保护小鼠免受实验性注射器传播的莱姆病螺旋体病感染。因此，研究了肩突硬蜱和鼠宿主内伯氏疏螺旋体bbk32和bbk50的表达，以及BBK32和BBK50抗血清在整个媒介-宿主生命周期中对螺旋体的影响。在饱血蜱中首次检测到bbk32和bbk50的mRNA和蛋白，表明在媒介内有调控的表达。然后，bbk32在小鼠接种部位的皮肤处表达增加。在小鼠播散性感染期间，bbk32和bbk50在几个小鼠组织中表达，30天时心脏和脾脏中的mRNA水平最高。BBK32抗血清可保护小鼠免受蜱传播的伯氏疏螺旋体感染，在叮咬免疫小鼠的若虫中螺旋体数量减少了90%。此外，这些蜱中有75%在蜕皮时不保留螺旋体，并损害了成年蜱随后的伯氏疏螺旋体传播。BBK32抗血清也抑制了肩突硬蜱幼虫对伯氏疏螺旋体的获取。这些数据表明，bbk32和bbk50在蜱饱血期间表达，并且BBK32抗血清可在媒介-宿主生命周期的各个阶段干扰螺旋体传播。这些研究为莱姆病螺旋体病和其他媒介传播疾病的免疫机制提供了深入了解。
