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Infection and Immunity, June 2002, p. 3208-3215, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3208-3215.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Fate of Entamoeba histolytica during Establishment of Amoebic Liver Abscess Analyzed by Quantitative Radioimaging and Histology

Marie-Christine Rigothier,¹ Hout Khun,² Paulo Tavares,^3,4, Ana Cardona,² Michel Huerre,² and Nancy Guillén^3,4*

Laboratoire de Biologie et Contrôle des Organismes Parasites, UPRES 398-IFR 75, Faculté de Pharmacie, Université Paris-Sud, Chatênay-Malabry,¹ Unité d'Histotechnologie et Pathologie,² Unité de Biologie Cellulaire du Parasitisme,³ Unité de Pathogénie Microbienne Moléculaire, Institut Pasteur, Paris 75724, Cedex 15, France⁴

Received 8 November 2001/ Returned for modification 21 December 2001/ Accepted 2 March 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.

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* Corresponding author. Mailing address: Unité de Biologie Cellulaire du Parasitisme and Unité de Pathogénie Microbienne Moléculaire, INSERM U389, Institut Pasteur, 28 Rue du Dr. Roux, Paris 75724, Cedex 15, France. Phone: 331-45-68-86-75. Fax: 331-45-68-86-74. E-mail: nguillen{at}pasteur.fr.

Editor: W. A. Petri, Jr.

Present address: Laboratoire de Génétique des Virus, CNRS, 91198 Gif-sur-Yvette Cedex, France.

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Infection and Immunity, June 2002, p. 3208-3215, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3208-3215.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

• Santi-Rocca, J., Rigothier, M.-C., Guillen, N. (2009). Host-Microbe Interactions and Defense Mechanisms in the Development of Amoebic Liver Abscesses. Clin. Microbiol. Rev. 22: 65-75 [Abstract] [Full Text]  
• Tavares, P., Rigothier, M.-C., Khun, H., Roux, P., Huerre, M., Guillen, N. (2005). Roles of Cell Adhesion and Cytoskeleton Activity in Entamoeba histolytica Pathogenesis: a Delicate Balance. Infect. Immun. 73: 1771-1778 [Abstract] [Full Text]