Department of Microbiology and Immunology, Center for Infectious Disease Research, Medical College of Wisconsin, Milwaukee, WI, USA.
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, USA.
Cell Microbiol. 2017 Dec;19(12). doi: 10.1111/cmi.12786. Epub 2017 Sep 26.
Borrelia burgdorferi (Bb) is the causative agent of Lyme disease in the United States, a disease that can result in carditis, and chronic and debilitating arthritis and/or neurologic symptoms if left untreated. Bb survives in the midgut of the Ixodes scapularis tick, or within tissues of immunocompetent hosts. In the early stages of infection, the bacteria are present in the bloodstream where they must resist clearance by the innate immune system of the host. We have found a novel role for outer surface protein C (OspC) from B. burgdorferi and B. garinii in interactions with the complement component C4b and bloodstream survival in vivo. Our data show that OspC inhibits the classical and lectin complement pathways and competes with complement protein C2 for C4b binding. Resistance to complement is important for maintenance of the lifecycle of Bb, enabling survival of the pathogen within the host as well as in the midgut of a feeding tick when ospC expression is induced.
伯氏疏螺旋体（Bb）是美国莱姆病的病原体，如果不治疗，该病可导致心炎、慢性和衰弱性关节炎和/或神经症状。Bb 存在于印鼠客蚤的中肠，或存在于免疫功能正常宿主的组织中。在感染的早期，细菌存在于血液中，必须抵抗宿主固有免疫系统的清除。我们发现伯氏疏螺旋体和伽氏疏螺旋体的外表面蛋白 C（OspC）在与补体成分 C4b 的相互作用以及体内血液生存方面具有新的作用。我们的数据表明，OspC 抑制经典和凝集素补体途径，并与补体蛋白 C2 竞争 C4b 结合。对补体的抗性对于维持 Bb 的生命周期很重要，使病原体能够在宿主内以及在 ospC 表达被诱导时的吸血蚤的中肠内生存。
