Phenotypic modulation of infiltrating macrophages in the myocardium during experimental infection with Trypanosoma cruzi

PONCE, NE; SANMARCO, LM; AOKI, MP

Mar del Plata

Congreso; LXI Reunion Anual de la Sociedad Argentina de Inmunologia; 2014

Sociedad Argentina de Inmunología

Emerging evidence points to the involvement of specialized immune cells as key drivers in the pathophysiology of cardiovascular diseases. Infection with T. cruzi is a major cause of morbidity and mortality in Latinamerica. Innate and adaptive immune response allow for control of parasite levels, but are insufficient to completely clear the infection and most individuals are infected for life, with parasites persisting primarily in muscle cells. Macrophages (Ma) are one of the main infiltrating leukocytes arriving to injured myocardium and they present two subtypes: M1 (inflammatory/antimicrobial) and M2 (immunoregulatory/healing). The aim of this study was to characterize the phenotypic modulation of Ma in murine cardiac tissue during the acute phase of the infection. We found that at early days post-infection (4dpi) M1 Ma (F4/80+CD68+CD86+CD206-) predominated over M2 (F4/80+CD68-CD86-CD206+) in infected Balb/c mice myocardium, but from 7dpi, Ma are sustained biased toward M2 phenotype throughout the acute infection (p