AOKI MARIA DEL PILAR
Congresos y reuniones científicas
Título:
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
Autor/es:
CABALEN, ME; SANMARCO, LM; EBERHARDT, N; CABRAL, MF; ANDRADA, MC; PONCE, NE; GEA S; AOKI, MP; CANO, RC
Reunión:
Congreso; Reunión conjunta de Sociedades de Biociencias; 2017
Resumen:
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
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
