Gentry-Weeks Claudia, Estay Monica, Loui Cindy, Baker Dale
Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado 80523, USA.
Infect Immun. 2003 Mar;71(3):1434-41. doi: 10.1128/IAI.71.3.1434-1441.2003.
An intravenous mouse infection model was used to compare the virulence of Enterococcus faecalis strains, to study bacterial localization and organ histopathology, and to examine the effects of Nramp1 and gamma interferon (IFN-gamma) on the course of infection. Infection of BALB/c mice with 5 x 10(8) CFU of E. faecalis JH2-2, MGH-2, 418, DS16C2, or OG1X revealed the following virulence ranking (from highest to lowest): MGH-2, 418, DS16C2, JH2-2, and OG1X. Discernible differences in the number of MGH-2 and JH2-2 bacteria were observed at 7 days (168 h) in the blood (P = 0.037), at 72 h in the liver (P = 0.002), and at 8 h in the spleen (P = 0.036). At these time points, the number of MGH-2 bacteria was higher in the blood and liver while the number of JH2-2 bacteria was higher in the spleen. At 72 h, livers from MGH-2-infected mice had higher numbers of coalescing aggregates of leukocytes and a greater degree of caseous necrosis than those from JH2-2-infected mice. These results indicate a correlation between the virulence of the E. faecalis strain, the number of bacteria in the liver, and the degree of histopathology of the liver at 72 h postinfection. IFN-gamma was important in E. faecalis infection, since IFN-gamma gene knockout mice had reduced mortality and massive coagulative necrosis was observed in wild-type mice. The contribution of Nramp1 was unclear, since Nramp1(-/-) mice and the respective control mice were innately resistant to E. faecalis. The mortality of mice in this model is probably due to induction of cytokine release and massive coagulative necrosis.
采用静脉注射小鼠感染模型来比较粪肠球菌菌株的毒力，研究细菌定位和器官组织病理学，并检测天然抗性巨噬细胞蛋白1（Nramp1）和γ干扰素（IFN-γ）对感染过程的影响。用5×10⁸CFU的粪肠球菌JH2-2、MGH-2、418、DS16C2或OG1X感染BALB/c小鼠，结果显示毒力排序如下（从高到低）：MGH-2、418、DS16C2、JH2-2和OG1X。在感染后7天（168小时）的血液中（P = 0.037）、72小时的肝脏中（P = 0.002）以及8小时的脾脏中（P = 0.036），观察到MGH-2和JH2-2细菌数量存在明显差异。在这些时间点，血液和肝脏中MGH-2细菌数量较多，而脾脏中JH2-2细菌数量较多。在72小时时，感染MGH-2的小鼠肝脏中白细胞融合聚集体数量更多，干酪样坏死程度比感染JH2-2的小鼠更高。这些结果表明粪肠球菌菌株的毒力、肝脏中的细菌数量与感染后72小时肝脏的组织病理学程度之间存在相关性。IFN-γ在粪肠球菌感染中起重要作用，因为IFN-γ基因敲除小鼠死亡率降低，且在野生型小鼠中观察到大量凝固性坏死。Nramp1的作用尚不清楚，因为Nramp1基因敲除小鼠和相应的对照小鼠对粪肠球菌天然耐药。该模型中小鼠的死亡可能是由于细胞因子释放的诱导和大量凝固性坏死。
