Marcinkiewicz Ashley L, Kraiczy Peter, Lin Yi-Pin
Division of Infectious Disease, Wadsworth Center, New York State Department of Health Albany, NY, USA.
Institute of Medical Microbiology and Infection Control, University Hospital of Frankfurt am Main Frankfurt am Main, Germany.
Front Microbiol. 2017 Mar 2;8:328. doi: 10.3389/fmicb.2017.00328. eCollection 2017.
Lyme disease and relapsing fever are caused by various species. Lyme disease , the most common vector-borne pathogens in both the U.S. and Europe, are transmitted by ticks and disseminate from the site of tick bites to tissues leading to erythema migrans skin rash, arthritis, carditis, and neuroborreliosis. Relapsing fever , carried by ticks and lice, trigger reoccurring fever episodes. Following transmission, spirochetes survive in the blood to induce bacteremia at the early stages of infection, which is thought to promote evasion of the host complement system. The complement system acts as an important innate immune defense mechanism in humans and vertebrates. Upon activation, the cleaved complement components form complexes on the pathogen surface to eventually promote bacteriolysis. The complement system is negatively modulated by a number of functionally diverse regulators to avoid tissue damage. To evade and inhibit the complement system, spirochetes are capable of binding complement components and regulators. Complement inhibition results in bacterial survival in serum (serum resistance) and is thought to promote bloodstream survival, which facilitates spirochete dissemination and disease manifestations. In this review, we discuss current methodologies to elucidate the mechanisms of spp. that promote serum resistance and bloodstream survival, as well as novel methods to study factors responsible for bloodstream survival of Lyme disease that can be applied to relapsing fever . Understanding the mechanisms these pathogens utilize to evade the complement system will ultimately aid in the development of novel therapeutic strategies and disease prevention to improve human health.
莱姆病和回归热由多种病原体引起。莱姆病是美国和欧洲最常见的媒介传播病原体，通过蜱虫传播，并从蜱虫叮咬部位扩散到组织，导致游走性红斑皮疹、关节炎、心脏炎和神经莱姆病。回归热由蜱虫和虱子传播，引发反复发热发作。传播后，螺旋体在血液中存活，在感染早期引发菌血症，这被认为有助于逃避宿主补体系统。补体系统是人类和脊椎动物重要的固有免疫防御机制。激活后，裂解的补体成分在病原体表面形成复合物，最终促进细菌溶解。补体系统受到多种功能各异的调节因子的负调控，以避免组织损伤。为了逃避和抑制补体系统，螺旋体能够结合补体成分和调节因子。补体抑制导致细菌在血清中存活（血清抗性），并被认为有助于在血液中存活，从而促进螺旋体的传播和疾病表现。在本综述中，我们讨论了阐明促进血清抗性和血液中存活机制的当前方法，以及研究莱姆病螺旋体血液中存活相关因素的新方法，这些方法可应用于回归热。了解这些病原体用于逃避补体系统的机制最终将有助于开发新的治疗策略和疾病预防方法，以改善人类健康。
