Shibayama M, Campos-Rodríguez R, Ramírez-Rosales A, Flores-Romo L, Espinosa-Cantellano M, Martínez-Palomo A, Tsutsumi V
Department of Experimental Pathology, CINVESTAV, Mexico, D.F., Mexico.
Exp Parasitol. 1998 Jan;88(1):20-7. doi: 10.1006/expr.1998.4218.
Intraperitoneal inoculation of axenically cultured Entamoeba histolytica trophozoites constitutes an easy to perform, highly reproducible procedure for inducing amebic liver abscesses in hamsters. Efficiency in abscess production (95% of infected animals after 1 week) was similar to data reported using direct intrahepatic or intraportal inoculation. The morphological sequence of infection shows that amebas in the peritoneal cavity initially produce a large exudate constituted mainly of acute inflammatory cells. These cells form a rim of polymorphonuclear leukocytes surrounding the amebas, which adhere to the trophozoite and can sometimes be observed polarized to one end of the parasite, suggesting capping of surface receptors. Early stages are also characterized by the production of distant inflammatory reactions in the hepatic portal spaces. At 6 h postintraperitoneal inoculation, larger foci of inflammatory reactions surrounding amebas are developed in the peritoneum, extending to and damaging the liver surface membranes as well as the serosa of other internal organs. Thereafter, tissue damage progresses deeper into the liver parenchyma, and a few days later, coalescing granulomas and large necrotic areas are observed in the liver tissue. Based on the present morphological time-sequence study, we suggest that inflammatory cells associated with E. histolytica trophozoites play an important role in commencing the damage of liver sheaths and producing the subsequent parenchymal lesions. The simplicity and reliability of this model are important factors to consider when large numbers of experimentally induced amebic liver abscesses are needed.
对无菌培养的溶组织内阿米巴滋养体进行腹腔接种,是在仓鼠中诱导阿米巴肝脓肿的一种易于操作且高度可重复的方法。脓肿形成效率(1周后95%的感染动物)与使用直接肝内或门静脉接种所报道的数据相似。感染的形态学序列显示,腹腔内的阿米巴最初产生主要由急性炎症细胞组成的大量渗出物。这些细胞形成围绕阿米巴的多形核白细胞边缘,其附着于滋养体,有时可观察到极化至寄生虫的一端,提示表面受体的封帽现象。早期还以肝门间隙出现远处炎症反应为特征。腹腔接种后6小时,腹膜内围绕阿米巴的更大炎症反应灶形成,延伸并损害肝表面膜以及其他内部器官的浆膜。此后,组织损伤向肝实质深部进展,几天后,在肝组织中观察到融合的肉芽肿和大的坏死区域。基于目前的形态学时间序列研究,我们认为与溶组织内阿米巴滋养体相关的炎症细胞在开始破坏肝包膜和产生随后的实质病变中起重要作用。当需要大量实验诱导的阿米巴肝脓肿时,该模型的简单性和可靠性是需要考虑的重要因素。