Feng H M, Wen J, Walker D H
Department of Pathology, University of Texas Medical Branch, Galveston 77555-0609.
Am J Pathol. 1993 May;142(5):1471-82.
A mouse model of spotted fever group rickettsiosis, in which disease results from disseminated rickettsial infection of endothelial cells and vascular damage, was developed by intravenous inoculation of 6- to 8-week-old, male, Balb/c mice with Rickettsia australis. Animals developed progressively severe vasculitis, interstitial pneumonia, and multifocal hepatic necrosis. These lesions correlated with early disseminated infection of endothelial cells followed by growth and invasion of rickettsiae into perivascular cells. The dose of 2 x 10(6) organisms was uniformly lethal. Serum interleukin- (IL) 1, IL-6, and interferon (IFN) increased by day 3 and tumor necrosis factor (TNF) on day 5. TNF, IL-6, and IFN declined on day 7. Spleen cells responded to Rickettsia australis antigen by producing IFN, TNF, IL-1, and IL-6 on day 5, followed by lower quantities of these cytokines on day 7. Despite the production of antibodies, IFN, TNF, IL-1, and IL-6, a lethal outcome occurred frequently. A decreased ability to secrete IL-2 suggests an element of infection-associated immunosuppression.
通过给6至8周龄的雄性Balb/c小鼠静脉接种澳大利亚立克次体，建立了斑点热群立克次体病的小鼠模型，该病是由内皮细胞的立克次体播散感染和血管损伤引起的。动物出现进行性加重的血管炎、间质性肺炎和多灶性肝坏死。这些病变与内皮细胞的早期播散感染相关，随后立克次体生长并侵入血管周围细胞。2×10⁶个菌体的剂量具有一致的致死性。血清白细胞介素（IL）-1、IL-6和干扰素（IFN）在第3天升高，肿瘤坏死因子（TNF）在第5天升高。TNF、IL-6和IFN在第7天下降。脾细胞在第5天通过产生IFN、TNF、IL-1和IL-6对澳大利亚立克次体抗原作出反应，随后在第7天这些细胞因子的量降低。尽管产生了抗体、IFN、TNF、IL-1和IL-6，但致死结局仍频繁发生。分泌IL-2的能力下降提示存在感染相关的免疫抑制因素。
