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Trypanosoma cruzi infection in humans and experimental animals causes Chagas disease which is often accompanied by myocarditis, cardiomyopathy and vasculopathy. T. cruzi-derived thromboxane A2 (TXA2) modulates vasculopathy and other pathophysiological features of Chagasic cardiomyopathy. Here, we provide evidence that epimastigotes, trypomastigotes and amastigotes of T. cruzi (Brazil and Tulahuen strains) express a biologically active thromboxane prostanoid (TP) receptor that is responsive to TXA2 mimetics, e.g. IBOP. This putative receptor, TcTP, is mainly localized in the flagellar membrane of the parasites and shows a similar glycosylation pattern to that of TPs obtained from human platelets. Furthermore, TXA2-TP signal transduction activates T. cruzi specific MAPK pathways. While mammalian TP is a G-protein coupled receptor (GPCR); T. cruzi genome sequencing has not demonstrated any GPCRs in these parasites. Based on this genome sequencing it is likely that TcTP is unique in these protists with no counterpart in mammals. TXA2 is a potent vasoconstrictor which contributes to the pathogenesis of Chagasic cardiovascular disease. It may, however, also control parasite differentiation and proliferation in the infected host allowing the infection to progress to a chronic state.

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