Rigothier Marie-Christine, Khun Hout, Tavares Paulo, Cardona Ana, Huerre Michel, Guillén Nancy
Laboratoire de Biologie et Contrôle des Organismes Parasites, UPRES 398-IFR 75, Faculté de Pharmacie, Université Paris-Sud, France.
Infect Immun. 2002 Jun;70(6):3208-15. doi: 10.1128/IAI.70.6.3208-3215.2002.
The protozoan parasite Entamoeba histolytica is the causative agent of amoebiasis, a human disease characterized by dysentery and liver abscess. The physiopathology of hepatic lesions can be satisfactorily reproduced in the hamster animal model by the administration of trophozoites through the portal vein route. Hamsters were infected with radioactively labeled amoebas for analysis of liver abscess establishment and progression. The radioimaging of material from parasite origin and quantification of the number inflammation foci, with or without amoebas, described here provides the first detailed assessment of trophozoite survival and death during liver infection by E. histolytica. The massive death of trophozoites observed in the first hours postinfection correlates with the presence of a majority of inflammatory foci without parasites. A critical point for success of infection is reached after 12 h when the lowest number of trophozoites is observed. The process then enters a commitment phase during which parasites multiply and the size of the infection foci increases fast. The liver shows extensive areas of dead hepatocytes that are surrounded by a peripheral layer of parasites facing inflammatory cells leading to acute inflammation. Our results show that the host response promotes massive parasite death but also suggest also that this is a major contributor to the establishment of inflammation during development of liver abscess.
原生动物寄生虫溶组织内阿米巴是阿米巴病的病原体,这是一种以痢疾和肝脓肿为特征的人类疾病。通过门静脉途径给予滋养体,可在仓鼠动物模型中令人满意地重现肝脏病变的生理病理学过程。用放射性标记的阿米巴感染仓鼠,以分析肝脓肿的形成和发展。本文所述的对源自寄生虫的物质进行放射性成像以及对有无阿米巴的炎症病灶数量进行量化,首次详细评估了溶组织内阿米巴感染肝脏期间滋养体的存活和死亡情况。感染后最初数小时观察到的滋养体大量死亡与大多数无寄生虫的炎症病灶的存在相关。感染成功的一个关键点在12小时后达到,此时观察到的滋养体数量最少。然后这个过程进入一个关键阶段,在此期间寄生虫繁殖,感染病灶的大小迅速增加。肝脏显示出广泛的肝细胞死亡区域,这些区域被一层面对炎症细胞的外周寄生虫层包围,导致急性炎症。我们的结果表明,宿主反应促进了大量寄生虫死亡,但也表明这是肝脓肿形成过程中炎症形成的主要因素。