Anais do Congresso Paranaense de Microbiologia
IV Congress of Microbiology in Paraná

The hemoflagellate protozoan Trypanosoma cruzi is the etiologic agent of Chagas Disease, which is considered a neglected tropical disease affecting approximately 7 million people worldwide. The parasite has a higher incidence in the shadowy regions of Latin America due to the presence of the insect vector responsible for its dissemination. However, the disease affects other regions of the world due to immigration, in addition to being transmitted by blood transfusion, organ donation, ingestion of contaminated food, in addition to other forms of spreading the disease. During infection caused by the parasite, the immune response developed by the host is important for the control of the parasitism, being necessary for survival. Macrophages are cells with recognized trypanocidal action, producing several inflammatory mediators such as eicosanoids, acting in the control of the parasite load and the development of the infection. However, the T. cruzi has evasion mechanisms, such as the extracellular vesicles (EVs), which participates in intercellular communication by carrying functional molecules that signal to host cells, modulating the immune response in its favor. Aspirin is classified as a non-steroidal anti-inflammatory that works by blocking the cyclooxygenase enzymes that are responsible for converting arachidonic acid into eicosanoids. Extracellular vesicles (EVs) shed by trypomastigote forms of Trypanosoma cruzi can interact with host tissues, increasing invasion, and modulating the host immune innate response. We have previously demonstrated that EVs shed by T. cruzi (Y strain) potentiates in vivo infection modulating the host response in favor of the parasite. In this study, the contribution of the host's cyclooxygenase (COX) enzyme on actions of EVs shed by T. cruzi (EVs-Y) in infected-RAW264.7 macrophages were investigated. RAW 264.7 cells exposed to EvY and later infected with trypomastigote forms of T. cruzi showed lower nitric oxide (NO) production and an increase in the number of amastigote forms internalized in the cell cytoplasm compared to controls (P < 0.05), indicating the modulation exerted by EvY to favor the parasite. Interestingly, when macrophages were treated with aspirin (0.625 mM), a dual COX inhibitor, before exposure to EvY, and subsequent trypomastigote infection, there was higher NO production as well as lower amastigote uptake compared to controls (P < 0.05). These results suggest that EVY modulates the macrophages response in favor of the T. cruzi and indicates a role for COX in immune modulation exerted by EVs.