Brieland J, Freeman P, Kunkel R, Chrisp C, Hurley M, Fantone J, Engleberg C
Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor.
Am J Pathol. 1994 Dec;145(6):1537-46.
The role of host immune responses in the pathogenesis of Legionnaires' disease is incompletely understood, due in part to the current lack of an animal model that is both susceptible to replicative Legionella pneumophila-induced lung infection and for which species-specific immunological reagents are available. We have developed a model of replicative L. pneumophila lung infection in intratracheally inoculated A/J mice. L. pneumophila was obtained in the exponential growth phase and inoculated into the trachea of 6- to 8-week-old female A/J mice. Microbiological and histopathological evidence of infection was demonstrated in mice inoculated with 10(6) colony-forming units. Development of an acute pneumonia that resembled human Legionnaires' disease coincided with exponential growth of the bacteria in the lung 24 to 48 hours after intratracheal inoculation of L. pneumophila. This was associated with increased plasma levels of interferon-gamma at 24 hours after inoculation. After 48 hours, the bacteria were gradually eliminated from the lung over the next 5 days, corresponding with resolution of the inflammatory response in the lung, thereby mimicking the outcome frequently seen in the immunocompetent human host. Treatment of animals with anti-interferon-gamma antibody enhanced bacterial replication and disease progression, indicating an important role of host immune response in resolution of the infection. Because of the availability of murine-specific reagents, this model of replicative L. pneumophila lung infection in A/J mice after intrapulmonary inoculation of L. pneumophila potentially provides an important tool for future studies investigating the role of host immune responses in the pathogenesis of Legionnaires' disease in the immunocompetent host.
宿主免疫反应在军团病发病机制中的作用尚未完全明确,部分原因是目前缺乏一种既易受嗜肺军团菌复制诱导的肺部感染影响,又有物种特异性免疫试剂可用的动物模型。我们建立了一种经气管内接种A/J小鼠的嗜肺军团菌复制性肺部感染模型。嗜肺军团菌在指数生长期获得,并接种到6至8周龄雌性A/J小鼠的气管中。接种10(6)个菌落形成单位的小鼠出现了感染的微生物学和组织病理学证据。在气管内接种嗜肺军团菌24至48小时后,类似于人类军团病的急性肺炎的发展与肺部细菌的指数生长同时发生。这与接种后24小时血浆中γ干扰素水平的升高有关。48小时后,细菌在接下来的5天内逐渐从肺部清除,这与肺部炎症反应的消退相对应,从而模拟了免疫功能正常的人类宿主中常见的结果。用抗γ干扰素抗体治疗动物可增强细菌复制和疾病进展,表明宿主免疫反应在感染消退中起重要作用。由于有小鼠特异性试剂,这种在肺内接种嗜肺军团菌后A/J小鼠的嗜肺军团菌复制性肺部感染模型可能为未来研究宿主免疫反应在免疫功能正常宿主的军团病发病机制中的作用提供重要工具。