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Infection and Immunity, March 2005, p. 1771-1778, Vol. 73, No. 3
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.3.1771-1778.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Roles of Cell Adhesion and Cytoskeleton Activity in Entamoeba histolytica Pathogenesis: a Delicate Balance

Paulo Tavares,1* Marie-Christine Rigothier,2 Huot Khun,3 Pascal Roux,4 Michel Huerre,3 and Nancy Guillén5*

Unité de Pathogénie Microbienne Moléculaire,1 Unité de Biologie Cellulaire du Parasitisme, INSERM U389,5 Unité d'Histotechnologie et Pathologie,3 Plateforme d'Imagerie Dynamique, Institut Pasteur, Paris,4 Laboratoire de Biologie et Contrôle des Organismes Parasites, UPRES 398-IFR 75, Faculté de Pharmacie, Université Paris-Sud, Chatênay-Malabry, France2

Received 21 June 2004/ Returned for modification 12 August 2004/ Accepted 11 November 2004

The protozoan parasite Entamoeba histolytica colonizes the human large bowel. Invasion of the intestinal epithelium causes amoebic colitis and opens the route for amoebic liver abscesses. The parasite relies on its dynamic actomyosin cytoskeleton and on surface adhesion molecules for dissemination in the human tissues. Here we show that the galactose/N-acetylgalactosamine (Gal/GalNAc) lectin clusters in focal structures localized in the region of E. histolytica that contacts monolayers of enterocytes. Disruption of myosin II activity impairs the formation of these structures and renders the trophozoites avirulent for liver abscess development. Production of the cytoplasmic domain of the E. histolytica Gal/GalNAc lectin in engineered trophozoites causes reduced adhesion to enterocytes. Intraportal delivery of these parasites to the liver leads to the formation of a large number of small abscesses with disorganized morphology that are localized in the vicinity of blood vessels. The data support a model for invasion in which parasite motility is essential for establishment of infectious foci, while the adhesion to host cells modulates the distribution of trophozoites in the liver and their capacity to migrate in the hepatic tissue.

* Corresponding author. Present address for Paulo Tavares: Unité de Virologie Moléculaire Structurale, BÂtiment 14B, CNRS, Avenue de la Terrasse, 91198 Gif-sur-Yvette Cedex, France. Phone: 331 69823860. Fax: 331 69824308. E-mail: tavares{at}vms.cnrs-gif.fr. Mailing address for Nancy Guillén: Unité de Biologie Cellulaire du Parasitisme, INSERM U389, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris Cedex 15, France. Phone: 331 45688675. Fax: 331 45688674. E-mail: nguillen{at}pasteur.fr.

* Corresponding author. Present address for Paulo Tavares: Unité de Virologie Moléculaire Structurale, BÂtiment 14B, CNRS, Avenue de la Terrasse, 91198 Gif-sur-Yvette Cedex, France. Phone: 331 69823860. . Fax: 331 69824308. E-mail: tavares{at}vms.cnrs-gif.fr. Mailing address for Nancy Guillén: Unité de Biologie Cellulaire du Parasitisme, INSERM U389, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris Cedex 15, France. Phone: 331 45688675. Fax: 331 45688674. E-mail: nguillen{at}pasteur.fr.

Editor: W. A. Petri, Jr.

Infection and Immunity, March 2005, p. 1771-1778, Vol. 73, No. 3
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.3.1771-1778.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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