Sebbane Florent, Gardner Donald, Long Daniel, Gowen Brian B, Hinnebusch B Joseph
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA.
Am J Pathol. 2005 May;166(5):1427-39. doi: 10.1016/S0002-9440(10)62360-7.
Plague, caused by the gram-negative bacterium Yersinia pestis, primarily affects rodents but is also an important zoonotic disease of humans. Bubonic plague in humans follows transmission by infected fleas and is characterized by an acute, necrotizing lymphadenitis in the regional lymph nodes that drain the intradermal flea bite site. Septicemia rapidly follows with spread to spleen, liver, and other organs. We developed a model of bubonic plague using the inbred Brown Norway strain of Rattus norvegicus to characterize the progression and kinetics of infection and the host immune response after intradermal inoculation of Y. pestis. The clinical signs and pathology in the rat closely resembled descriptions of human bubonic plague. The bacteriology; histopathology; host cellular response in infected lymph nodes, blood, and spleen; and serum cytokine levels were analyzed at various times after infection to determine the kinetics and route of disease progression and to evaluate hypothesized Y. pestis pathogenic mechanisms. Understanding disease progression in this rat infection model should facilitate further investigations into the molecular pathogenesis of bubonic plague and the immune response to Y. pestis at different stages of the disease.
鼠疫由革兰氏阴性细菌鼠疫耶尔森氏菌引起，主要感染啮齿动物，但也是一种重要的人畜共患病。人类的腺鼠疫通过受感染的跳蚤传播，其特征是在引流皮内跳蚤叮咬部位的局部淋巴结出现急性坏死性淋巴结炎。随后迅速发展为败血症，并扩散至脾脏、肝脏和其他器官。我们使用近交系挪威棕色大鼠（Rattus norvegicus）建立了腺鼠疫模型，以描述皮内接种鼠疫耶尔森氏菌后感染的进展和动力学以及宿主免疫反应。大鼠的临床症状和病理学与人类腺鼠疫的描述极为相似。在感染后的不同时间分析细菌学、组织病理学、感染淋巴结、血液和脾脏中的宿主细胞反应以及血清细胞因子水平，以确定疾病进展的动力学和途径，并评估假定的鼠疫耶尔森氏菌致病机制。了解这种大鼠感染模型中的疾病进展应有助于进一步研究腺鼠疫的分子发病机制以及疾病不同阶段对鼠疫耶尔森氏菌的免疫反应。
