Dierberg Kerry L, Dumler J Stephen
Division of Medical Microbiology, Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
BMC Infect Dis. 2006 Jul 21;6:121. doi: 10.1186/1471-2334-6-121.
Human monocytic ehrlichiosis (HME) and Rocky Mountain spotted fever (RMSF) are caused by Ehrlichia chaffeensis and Rickettsia rickettsii, respectively. The pathogenesis of RMSF relates to rickettsia-mediated vascular injury, but it is unclear in HME.
To study histopathologic responses in the lymphatic system for correlates of immune injury, lymph nodes from patients with HME (n = 6) and RMSF (n = 5) were examined. H&E-stained lymph node tissues were examined for five histopathologic features, including hemophagocytosis, cellularity, necrosis, and vascular congestion and edema. The relative proportions of CD68 macrophages, CD8 and CD4 T lymphocytes, and CD20 B lymphocytes were evaluated by immunohistochemical staining.
Hemophagocytosis was similar in HME and RMSF, and was greater than in control cases (p = .015). Cellularity in HME was not different from controls, whereas RMSF lymph nodes were markedly less cellular (p < 0.002). E. chaffeensis-infected mononuclear phagocytes were infrequent compared to R. rickettsii-infected endothelial cells. More CD8 cells in lymph nodes were observed with HME (p < .001), but no quantitative differences in CD4 lymphocytes, macrophages, or B lymphocytes were identified.
Hemophagocytosis, CD8 T cell expansion, and the paucity of infected cells in HME, suggest that E. chaffeensis infection leads to macrophage activation and immune-mediated injury.
人单核细胞埃立克体病(HME)和落基山斑疹热(RMSF)分别由恰菲埃立克体和立氏立克次体引起。RMSF的发病机制与立克次体介导的血管损伤有关,但HME的发病机制尚不清楚。
为研究淋巴系统中的组织病理学反应以寻找免疫损伤的相关因素,对HME患者(n = 6)和RMSF患者(n = 5)的淋巴结进行了检查。对苏木精-伊红(H&E)染色的淋巴结组织检查了五个组织病理学特征,包括噬血细胞现象、细胞密度、坏死以及血管充血和水肿。通过免疫组织化学染色评估CD68巨噬细胞、CD8和CD4 T淋巴细胞以及CD20 B淋巴细胞的相对比例。
HME和RMSF中的噬血细胞现象相似,且高于对照病例(p = 0.015)。HME中的细胞密度与对照无差异,而RMSF淋巴结的细胞密度明显较低(p < 0.002)。与立氏立克次体感染的内皮细胞相比,恰菲埃立克体感染的单核吞噬细胞较少见。HME患者淋巴结中观察到更多的CD8细胞(p < 0.001),但在CD4淋巴细胞、巨噬细胞或B淋巴细胞中未发现数量差异。
HME中的噬血细胞现象、CD8 T细胞扩增以及感染细胞的缺乏,提示恰菲埃立克体感染导致巨噬细胞活化和免疫介导的损伤。