Leishmaniosis and Chagas disease are neglected tropical disease caused by flagellate protozoa from Trypanosomatidae family and transmitted to humans from insect vectors. During cellular invasion by different evolutionary forms of these parasites, is observed a biogenesis of parasitophorous vacuole (PV), which is the structure that shelter parasite within the host cells. These structures develops as phagolysosomes, maturing from fusion with primaries endosomes, secondaries endosomes and lysosomes. Each intracellular parasite "customize" in which VP is shelter, as subverting the host vesicular traffic or restricting the passage of components (such as enzymes and protons) to the contents of the vacuole. The intracellular coinfection involving these two pathogens generates chimeric vacuoles that shelter these two parasites concomitantly. This study aims to investigate the coinfection between L. (L.) amazonensis and T. cruzi in primary macrophages and lineage in order to investigate the influence of a vacuole customized by the first pathogen survival and differentiation of the second. The function of components involved in the biogenesis of PVs of L. amazonensis and T. cruzi as well as the formation of chimeric vacuole will be investigate from the technique of RNA interferential for the genes vacuolar ATPase, Rab GTP ases, SNAREs and lysosome-associated proteins (LAMPs). Our study will allow the evaluation of the interference and interaction between different pathogens that share the same cytoplasmic environment and / or vacuolar in host cell.
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