Efeitos de molécula sintética na dinâmica Trypanosoma cruzi-hospedeiro

Abstract

Chagas disease is an illness caused by the protozoan Trypanosoma cruzi, transmitted mainly through contact with the infected feces released by triatomine insects after the bite. The disease evolves through acute and chronic phases and can lead to severe cardiac and digestive complications. Despite scientific advances, treatment remains limited due to the toxicity of the available drugs and their low efficacy in the chronic stage. In this context, understanding the molecular mechanisms of infection is essential for developing new therapeutic strategies. The Brazilian biodiversity offers a wide source of bioactive compounds with pharmacological potential, including insect venoms. Among them, the synthetic molecule PEP A, derived from the venom of the ant Ectatomma tuberculatum, was used in this study as an experimental model to evaluate its activity against T. cruzi. The aim of this work was to investigate the effects of this synthetic molecule on cell viability, parasite invasion, and intracellular multiplication. For this purpose, LLC-MK2 mammalian cells were used as host cells and T. cruzi Tulahuen strain tissue culture-derived trypomastigotes as infective forms. Viability assays were performed on both host cells and parasites, along with invasion and intracellular multiplication experiments, in order to explore different stages of the host–parasite interaction. The results demonstrated that, although PEP A did not exhibit direct trypanocidal activity or significant cytotoxicity to host cells, it interfered with key steps of the host–parasite interaction, reducing cell invasion, possibly by modulating parasite surface molecules such as GP82, GP85, trans-sialidases, and mucins. Therefore, this study contributes to a better understanding of T. cruzi–host cell interactions and highlights the potential of bioactive compounds from Brazilian biodiversity as promising tools in the search for new therapeutic approaches for Chagas disease.