Baker-Zander S, Sell S
Am J Pathol. 1980 Nov;101(2):387-414.
Inoculation of the causative agent of syphilis, Treponema pallidum into the testes of rabbits initiated the following sequence of events: 1) a rapid proliferation of organisms in the interstitial tissues of the testes, reaching a maximum at about 10-11 days after infection; 2) systemic spread of organisms primarily in the lymphoid organs; 3) a prompt immune response manifested by hyperplasia of T cell domains in draining lymph nodes and spleen, blast transformation responses of lymphoid cells to sonicates of T pallidum, the appearance of serum antibody, and the marked infiltration of the infected areas of the testes by T cells; 4) essential clearing of organisms identified by immunofluorescence from the infected site 10-14 days after infection associated with evolution of the inflammatory response from primarily a T cell infiltrate to a larger mononuclear cell type, and the immunofluorescent identification of presumptive T pallidum antigen in macrophages; 5) interstitial fibrosis or resolution 17-21 days after infection so that examination of infected testes from 1 to 24 months later reveals foci of tubular atrophy and fibrosis of varying size, alternating with regenerated tubules, separated by interstitial areas with only minimal fibrosis. During the long period of latency there is no evidence of atrophy or hypoplasia of the lymphoid organs and long-lasting T cell memory with regard to T pallidum sonicates is demonstrable. Reinfection of previously inoculated rabbits indicates partial protection at 25 days after infection followed by essentially complete protection after 55 days. It is concluded that there is a prompt and long-lasting immune response to T pallidum in experimentally infected rabbits. The main mechanism for destruction of infecting organisms appears to be T-cell-initiated macrophage-mediated destruction, but a role for antibody dependent phagocytosis cannot be ruled out. The reason that some organisms may survive in various body organs remains unknown, but possible explanations are presented.
1）病原体在睾丸间质组织中迅速增殖，在感染后约10 - 11天达到高峰；2）病原体主要在淋巴器官中进行全身扩散；3）迅速出现免疫反应，表现为引流淋巴结和脾脏中T细胞区域增生、淋巴细胞对苍白密螺旋体超声裂解物的母细胞转化反应、血清抗体出现以及T细胞对睾丸感染区域的显著浸润；4）感染后10 - 14天，通过免疫荧光法确定感染部位的病原体基本清除，同时炎症反应从主要的T细胞浸润演变为更大的单核细胞类型，并在巨噬细胞中通过免疫荧光法鉴定出推定的苍白密螺旋体抗原；5）感染后17 - 21天出现间质纤维化或消退，因此在感染后1至24个月检查感染的睾丸时，会发现大小不一的管状萎缩和纤维化病灶，与再生的小管交替出现，被仅有轻微纤维化的间质区域分隔开。在漫长的潜伏期内，没有证据表明淋巴器官出现萎缩或发育不全，并且对于苍白密螺旋体超声裂解物具有持久的T细胞记忆是可证明的。对先前接种过的兔子进行再次感染表明，在感染后25天有部分保护作用，55天后基本完全得到保护。得出的结论是，在实验感染的兔子中，对苍白密螺旋体存在迅速且持久的免疫反应。破坏感染病原体的主要机制似乎是T细胞启动的巨噬细胞介导的破坏，但不能排除抗体依赖性吞噬作用的作用。一些病原体可能在身体各个器官中存活的原因仍然未知，但提出了一些可能的解释。
