Study of the early events in the Trypanosoma cruzi invasion.

ARBOIT MA, RIVERO CV, COLOMBO MI, ROMANO PS

Mendoza. Argentina.

Congreso; XXVI Reunión Científica Anual de la Sociedad de Biología de Cuyo. I Reunión Dirección Investigación, Ciencia y Técnica. Ministerio de Salud – Gobierno de Mendoza.; 2008

Sociedad de Biología de Cuyo

Trypanosoma cruzi, the etiologic agent of Chagas disease, invades a wide range of phagocytic and non-phagocytic cells by means of the infective trypomastigote form. Our group has demonstrated previously that T. cruzi interacts with the autophagic pathway during infection and that the induction of autophagy significantly increased the percentage of infected cells at 1-6 h after infection. Moreover autophagy induction increases the association between this parasite and Lamp-1, a protein that localize in lysosomes. The localization of T. cruzi and autophagosomes/autophagolysosomes were then confirmed by live cell imaging experiments. We next study the connection between the parasite vacuole and VAMP-7, a SNARE protein that associate with autophagosomes.  Using CHO cells overespressing GFP-VAMP-7, we observed by confocal microscopy a colocalization between the parasitophorous vacuole and this protein whereas in cells overexpressing GFP-VAMP-7-NT, a non-functional protein, no localization was observed. We conclude that autophagic pathway is a key component in the lysosomal dependent entry of Trypanosoma cruzi into the host cell. Furthermore, fusion proteins like Synaptotagmin VII and VAMP-7 are implicated in the fusion process between autophagosomes and the plasma membrane.