CONICET | Buscador de Institutos y Recursos Humanos

Chagas´ disease is caused by the protozoa Trypanosoma cruzi , which has a complex biologicalcycle. To succeed the infection, T. cruzi presents several mechanisms to escape the immunesystem and to invade eukaryotic cells, expressing different molecules and releasingextracellular vesicles. Extracellular vesicles (EVs) are small vesicles composed of a lipid bilayerwhich comprises microvesicles and exosomes, according to their size and biogenesis. Our group have shown the release of EVs during the interaction between the parasite and host cellspromotes complement system inhibition and increases the invasion of metacyclic forms tocells. Here, our aim was to understand the secretion of EVs by different stages of the parasite inthe interaction with mammalian cells and how these EVs could manipulate host immunesystem. Parasites from CL Brener and Dm28 strains of T. cruzi was differentiate to metacyclicforms (METAs) by a nutrient starvation process and tissue-culture derived trypomastigotes(TCT) was obtained from supernatant of infected VERO cells monolayers. To induce EVssecretion, the different stages from the parasites was exposed to THP1 cells in a relation of 5:1(parasites:cells) for one hour at 37°C. Subpopulations of EVs was isolated by differentialcentrifugation method, with large EVs (LEVs, predominantly microvesicles) obtained from a11.000 xg centrifugation and small EVs (SEVs, predominantly exosomes) from a subsequent100.000 xg centrifugation. The two subpopulations of EVs was differentially secreted from theparasites and had different features. Moreover, it was seen that EVs from different strains wascapable of inducing a cytokine response in dendritic cells, acting as communicators during theinfection and modulating the immune system. The next steps of this work is to understand ifEVs from METAs or TCTs plays different roles, since different infectious forms face differentscenarios during the infection.