Martin M E, Bunnell J E, Dumler J S
Department of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
J Infect Dis. 2000 Jan;181(1):374-8. doi: 10.1086/315206.
Human granulocytic ehrlichiosis (HGE) results in fever, pancytopenia, and mild liver injury. We used a mouse model to examine immunity in the pathogenesis of HGE. HGE agent-infected C3H/HeJ mice were necropsied over 21 days. Histologic, immunohistologic, and serologic analyses, blood culture, tissue and blood polymerase chain reaction (PCR), cell counts, serum chemistries, and plasma cytokine ELISAs were performed. No clinical signs were detected. Ehrlichiae were identified in neutrophils in hematopoietic tissues maximally on day 7. Interleukin (IL)-10 levels were high throughout, whereas interferon (IFN)-gamma levels peaked on days 7 and 10 and dropped thereafter. Hepatic lymphohistiocytic aggregates with apoptoses were maximal at day 14. HGE-agent infection of mice induces pathologic changes similar to those in infected humans, despite differences in cytokine profile. The IFN-gamma peak prior to maximal pathologic change, when ehrlichiae are absent in tissues, suggests a role for host immunity in the pathogenesis of HGE.
人粒细胞埃立克体病（HGE）可导致发热、全血细胞减少和轻度肝损伤。我们使用小鼠模型来研究HGE发病机制中的免疫情况。对感染HGE病原体的C3H/HeJ小鼠在21天内进行尸检。进行了组织学、免疫组织学和血清学分析、血培养、组织和血液聚合酶链反应（PCR）、细胞计数、血清化学分析以及血浆细胞因子酶联免疫吸附测定（ELISA）。未检测到临床症状。在第7天时，造血组织中的中性粒细胞中最多地鉴定出埃立克体。白细胞介素（IL）-10水平始终较高，而干扰素（IFN）-γ水平在第7天和第10天达到峰值，此后下降。伴有凋亡的肝淋巴细胞组织细胞聚集在第14天达到最大值。尽管细胞因子谱存在差异，但小鼠感染HGE病原体诱导的病理变化与感染人类时相似。在最大病理变化之前，即组织中不存在埃立克体时IFN-γ达到峰值，这表明宿主免疫在HGE发病机制中起作用。
