ABSTRACT
Trypanosoma cruzi
is a protozoan parasite that causes Chagas disease (CD). CD is a persistent, lifelong infection affecting many organs, most notably the heart, where it may result in acute myocarditis and chronic cardiomyopathy. The pathological features include myocardial inflammation and fibrosis. In the Brazil strain-infected CD-1 mouse, which recapitulates many of the features of human infection, we found increased plasma levels of resolvin D1 (RvD1), a specialized proresolving mediator of inflammation, during both the acute and chronic phases of infection (>100 days postinfection) as determined by enzyme-linked immunosorbent assay (ELISA). Additionally, ELISA on lysates of trypomastigotes of both strains Tulahuen and Brazil revealed elevated levels of RvD1 compared with lysates of cultured epimastigotes of
T. cruzi
, tachyzoites of
Toxoplasma gondii
, trypomastigotes of
Trypanosoma brucei
, cultured L
6
E
9
myoblasts, and culture medium containing no cells. Lysates of
T. cruzi
-infected myoblasts also displayed increased levels of RvD1. Lipid mediator metabolomics confirmed that the trypomastigotes of
T. cruzi
produced RvD1, RvD5, and RvE2, which have been demonstrated to modulate the host response to bacterial infections. Plasma RvD1 levels may be both host and parasite derived. Since
T. cruzi
synthesizes specialized proresolving mediators of inflammation, as well as proinflammatory eicosanoids, such as thromboxane A
2
, one may speculate that by using these lipid mediators to modulate its microenvironment, the parasite is able to survive.
Molecular ecology of Triatoma dimidiata in southern Belize reveals risk for human infection and the local differentiation of Trypanosoma cruzi parasites
