CHAGAS DISEASE IN AN OBESOGENIC CONTEXT: A HIGHLIGHT ROLE FOR VISCERAL ADIPOSE TISSUE AS A CHRONIC RESERVOIR OF Trypanosoma cruzi THAT CONTRIBUTES TO ASSOCIATED CARDIOVASCULAR COMPLICATIONS

CABALEN, ME; SANMARCO, LM; EBERHARDT, N; CABRAL, MF; ANDRADA, MC; PONCE, NE; GEA S; AOKI, MP; CANO, RC

Congreso; Reunión conjunta de Sociedades de Biociencias; 2017

Chagas disease and obesity are chronic and public health concerns with associated cardiovascular complications (CV). Oxidative stress  (OS)  and  inflammation  are  common  mechanisms  that  predispose to CV. We hypothesize that in an obesogenic context, the immune-metabolic dysregulation exerted by T. cruziinfection could drive CV. To elucidate this complex interrelation, we evaluate the lipid and lipoprotein systemic changes and the oxidative and immune-inflammatory alterations in visceral adipose tissue (VAT) in uninfected C57BL/6 mice feed with LFD (4% fat diet) or DIO (14% fat/ 5% fructose diet), or infected (LFD+I and DIO+I) groups. Although an improvement  on  plasma  triglycerides  (TG)  and  total  cholesterol (TC) levels were seen in DIO+I compared to DIO mice (p<0.001; p<0.001), apoB100 levels were increased in all groups in relation to LFD (p< 0.05); suggesting the presence of atherogenic small and dense LDL particles in infected groups. Concomitant qualitative differences in lipoprotein bands were observed. Significant decreases in the adiponectin levels were seen in both infected groups compared  to  DIO  and  LFD  (p<0.001;  p<0.001).  In  VAT,  inflammatory cell-infiltration (p<0.001) and OS (measured by lipid peroxidation) were exacerbated in DIO+I compared to LFD+I mice (p<0.05). Despite a higher number of macrophages observed in VAT (ATM) from DIO+I than in LFD+I mice (p<0.001), they presented a M2 phenotype  (F4/80+CD11c-CD206+).  Furthermore,  increased  CD36  expression (p<0.05) and parasite load (p<0.05) was seen in VAT from DIO+I compared to LFD+I. Conversely in heart, a low parasite load was observed independent of the diet, highlighting VAT as a more suitable chronic reservoir.The strong inflammatory and oxidative response in an obesogenic context is probably counter-balanced by the parasite, which may induce the polarization of ATM to a M2 phenotype to favor its own survival. Thus, parasite persistence would be a key trigger in the progression of CV Chagas disease