Microvesicles released during the interaction between Trypanosoma cruzi TcI and TcII strains and host blood cells inhibit complement system and increase the infectivity of metacyclic forms of host cells in a strain-independent process.

Abstract

Extracellular vesicles, whether microvesicles (MVs) or exosomes, shed by pathogens transfer virulence factors and biomolecules to host cells, thereby altering the host's susceptibility to infection. We have previously demonstrated that MV release is increased during the interaction between the infective forms of Trypanosoma cruzi and host cells. MVs confer parasite resistance to complement-mediated lysis and enhance parasite invasion. In this study, we show that differences exist in the levels of MVs released during the interaction between metacyclic trypomastigotes of different T. cruzi strains (with varied sensitivity to complement-mediated lysis, namely sensitive G strain TcI and resistant Y strain TcII) and host cells. MVs produced during the interaction between TcII parasites and host cells increased parasite resistance to complement lysis from 50% to 80% and parasite invasion was increased to over 50%. MVs purified during the interaction between TcI parasites and host cells have a stronger effect, doubling complement resistance and parasite invasion. The complement-mediated lysis assays showed that all MVs inhibit mainly the lectin pathway. Interestingly, MVs derived from parasites of one class did not alter complement resistance and the invasion process of parasites from the other class. This is the first description of MVs from T. cruzi with strain-dependent phenotypic effects.