Chronic Trypanosoma cruziinfection potentiates adipose tissue macrophage polarization toward an anti-inflammatory M2 phenotype and contributes to diabetes progression in a dietinduced obesity model

CABALEN, ME; CABRAL, MF; SANMARCO, LM; ANDRADA, MC; ONOFRIO, L; PONCE, NE; AOKI, MP; GEA, SUSANA; CANO, RC

ONCOTARGET

Oncotarget eiditorial

Año: 2016

hronic obesity and Chagas disease (caused by the protozoan Trypanosoma cruzi) represent serious public health concerns. The interrelation between parasite infection, adipose tissue, immune system and metabolism in an obesogenic context, has  not  been  entirely  explored.  A  novel  diet-induced  obesity  model  (DIO)  was developed  in  C57BL/6  wild  type  mice  to  examine  the  effect  of  chronic  infection (DIO+I) on metabolic parameters and on obesity-related disorders. Dyslipidemia, hyperleptinemia,  and  cardiac/hepatic  steatosis  were  strongly  developed  in  DIO mice. Strikingly, although these metabolic alterations were collectively improved by  infection,  plasmatic  apoB100  levels  remain  significantly  increased  in  DIO+I