TRYPANOSOMA CRUZI PROMOTES VASCULAR ALTERATIONS ASSOCIATED WITH RISK OF CARDIOVASCULAR DISEASE

VOLPINI, XIMENA; BRUGO, MARÍA BELEN; NATALI, L; DE LA CRUZ, T; CLAUDIA MOTRAN; MUSRI, M

Virtual

Congreso; Reunión anual de Sociedades de Biociencias; 2020

SAI-SAIC

Chagas disease, caused by the parasite Trypanosoma cruzi, is an important cause of cardiac disease in endemic areas of Latin Amer- ica. About 35% of infected patients develop chronic myocardiopathy that can lead to cardiac failure and stroke. The other infected patients remain asymptomatic (indetermined form), although increased aorta stiffness (AS) has been described in all infected patients suggesting that the infection could contribute to vascular alterations. Despite the importance of the vasculature in regulating the homeostasis of the cardiovascular system, little is known about its changes in re- sponse to this infection. The aim of this work was to study vascular cell population changes during the acute phase of T. cruzi infection. Thoracic (Athor), abdominal aorta (Aabd), aortic arch, and brachio- cephalic artery (BCA) were obtained from BALB/c mice infected with 500 tps of T. cruzi at day 16 post-infection with non-infected mice (NI) used as controls. Arterial segments were analyzed by multi- parametric FACS followed by t-SNE analysis to identify different cell populations. Similar cell clusters were observed in BCA, Aabd, and arch but not in Athor of NI mice. In addition, Athor was the segment presenting the major differences in cell clusters composition after infection. Thus, T. cruzi infection increased the percent of α-SMA+ (smooth muscle cells, SMC) and F4/80+ CD11b+ (macrophages, Mo) cells, and the expression of markers of active immune cells. Interestingly, cell clusters co-expressing SMC- and Mo-markers, suggesting SMC-transdifferentiation into Mo or viceversa, were also observed in Athor. Taken together, these results suggest that T. cruzi infection induces vascular changes, being Athor the most affected segment. Besides, transdifferentiation and immune cell activation could be mechanisms involved in these vascular alterations.