Abstract

Author summaryChagas disease is prevalent in Latin America and is widely distributed worldwide due to migration. In 30% of patients, if the parasite is left untreated, the disease may progress from an acute symptomless phase to chronic myocardial inflammation, which can cause heart failure and death, years after the infection. Imbalances in the inflammatory response are related to this progression. Current treatments cannot prevent or reverse the cardiac damage inflicted by the parasite. Aspirin-triggered resolvin D1, also named AT-RvD1, can modify cellular and humoral inflammatory responses leading to the resolution of inflammation, thus promoting healing and restoring organ function. In this study, AT-RvD1, in an N-formyl peptide receptor 2 (FPR2)-dependent manner, was shown to regulate local and systemic inflammation and decrease cellular infiltration in the heart tissue of mice chronically infected with the parasite and reduce cardiac hypertrophy and fibrosis in the early stages of the chronic phase of the disease. Importantly, AT-RvD1 was able to decrease parasite load in the infected hearts. Thus, this research indicates that At-RvD1 treatment is a potential therapeutic strategy that offers an improvement on current drug therapies.