Osterloh Anke, Papp Stefanie, Moderzynski Kristin, Kuehl Svenja, Richardt Ulricke, Fleischer Bernhard
Department of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany
Department of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.
Infect Immun. 2016 Apr 22;84(5):1615-1632. doi: 10.1128/IAI.00034-16. Print 2016 May.
Rickettsioses are emerging febrile diseases caused by obligate intracellular bacteria belonging to the family Rickettsiaceae. Rickettsia typhi belongs to the typhus group (TG) of this family and is the causative agent of endemic typhus, a disease that can be fatal. In the present study, we analyzed the course of R. typhi infection in C57BL/6 RAG1(-/-) mice. Although these mice lack adaptive immunity, they developed only mild and temporary symptoms of disease and survived R. typhi infection for a long period of time. To our surprise, 3 to 4 months after infection, C57BL/6 RAG1(-/-) mice suddenly developed lethal neurological disorders. Analysis of these mice at the time of death revealed high bacterial loads, predominantly in the brain. This was accompanied by a massive expansion of microglia and by neuronal cell death. Furthermore, high numbers of infiltrating CD11b(+) macrophages were detectable in the brain. In contrast to the microglia, these cells harbored R. typhi and showed an inflammatory phenotype, as indicated by inducible nitric oxide synthase (iNOS) expression, which was not observed in the periphery. Having shown that R. typhi persists in immunocompromised mice, we finally asked whether the bacteria are also able to persist in resistant C57BL/6 and BALB/c wild-type mice. Indeed, R. typhi could be recultivated from lung, spleen, and brain tissues from both strains even up to 1 year after infection. This is the first report demonstrating persistence and reappearance of R. typhi, mainly restricted to the central nervous system in immunocompromised mice.
立克次氏体病是由立克次氏体科专性细胞内细菌引起的新兴发热性疾病。鼠型斑疹伤寒立克次氏体属于该科的斑疹伤寒群(TG),是地方性斑疹伤寒的病原体,这种疾病可能致命。在本研究中,我们分析了鼠型斑疹伤寒立克次氏体在C57BL/6 RAG1(-/-)小鼠中的感染过程。尽管这些小鼠缺乏适应性免疫,但它们仅出现了轻微和暂时的疾病症状,并在鼠型斑疹伤寒立克次氏体感染后长期存活。令我们惊讶的是,感染后3至4个月,C57BL/6 RAG1(-/-)小鼠突然出现致命的神经紊乱。在这些小鼠死亡时进行分析发现,细菌载量很高,主要集中在大脑。这伴随着小胶质细胞的大量扩增和神经元细胞死亡。此外,在大脑中可检测到大量浸润的CD11b(+)巨噬细胞。与小胶质细胞不同,这些细胞携带鼠型斑疹伤寒立克次氏体,并表现出炎症表型,如诱导型一氧化氮合酶(iNOS)表达所示,在外周未观察到这种情况。在证明鼠型斑疹伤寒立克次氏体在免疫受损小鼠中持续存在后,我们最终询问这些细菌是否也能够在抗性C57BL/6和BALB/c野生型小鼠中持续存在。事实上,即使在感染后长达1年,仍可从这两种品系的肺、脾和脑组织中再次培养出鼠型斑疹伤寒立克次氏体。这是第一份证明鼠型斑疹伤寒立克次氏体持续存在和再次出现的报告,主要局限于免疫受损小鼠的中枢神经系统。