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Clinical Microbiology Reviews, January 2009, p. 65-75, Vol. 22, No. 1
0893-8512/09/$08.00+0     doi:10.1128/CMR.00029-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Host-Microbe Interactions and Defense Mechanisms in the Development of Amoebic Liver Abscesses

Julien Santi-Rocca,1,2 Marie-Christine Rigothier,3 and Nancy Guillén1,2*

Institut Pasteur, Unité Biologie Cellulaire du Parasitisme, Paris, France,1 INSERM U 786, Paris, France,2 Université Paris-Sud, Faculté de Pharmacie, Laboratoire de Biologie et Contrôle des Organismes Parasites, Châtenay-Malabry, France3

Summary: Amoebiasis by Entamoeba histolytica is a major public health problem in developing countries and leads to several thousand deaths per year. The parasite invades the intestine (provoking diarrhea and dysentery) and the liver, where it forms abscesses (amoebic liver abscesses [ALAs]). The liver is the organ responsible for filtering blood coming from the intestinal tract, a task that implies a particular structure and immune features. Amoebae use the portal route and break through the sinusoidal endothelial barrier to reach the hepatic parenchyma. When faced with systemic and cell-mediated defenses, trophozoites adapt to their new environment and modulate host responses, leading to parasite survival and the formation of inflammatory foci. Cytopathogenic effects and the onset of inflammation may be caused by diffusible products originating from parasites and/or immune cells either by their secretion or by their release after cell death. Liver infection thus results from the interplay between E. histolytica and hepatic cells. Despite its importance in terms of public health burden, the lack of integrated data on ALA genesis means that we have only an incomplete description of the initiation and development of hepatic amoebiasis. Here, we review the main steps of ALA development as well as the responses triggered in both the host and the parasite. Transcriptome studies highlighted parasite factors involved in adherence to human cells, cytopathogenic effects, and adaptative and stress responses. An understanding of their role in ALA development will help to unravel the host-pathogen interactions and their evolution throughout the infection.

* Corresponding author. Mailing address: Unité Biologie Cellulaire du Parasitisme, Institut Pasteur, 28 Rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: 331-45688675. Fax: 331-45688674. E-mail: nguillen{at}pasteur.fr

Clinical Microbiology Reviews, January 2009, p. 65-75, Vol. 22, No. 1
0893-8512/09/$08.00+0     doi:10.1128/CMR.00029-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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