Chronic Trypanosoma cruzi infection potentiates adipose tissue macrophage polarization toward an anti-inflammatory M2 phenotype and contributes to diabetes progression in a diet-induced obesity model

Autor: María Fernanda Cabral, Liliana Maria Sanmarco, Nicolás Eric Ponce, María Eugenia Cabalén, Susana Gea, Marta Cecilia Andrada, Roxana Carolina Cano, Maria del Pilar Aoki, Luisina I. Onofrio
Rok vydání: 2016
Předmět:
Male
0301 basic medicine
obesity
immunometabolism
Anti-Inflammatory Agents
Adipose tissue
030204 cardiovascular system & hematology
Mice
0302 clinical medicine
innate immunity
Cells
Cultured

Research Paper: Immunology
purl.org/becyt/ford/3.1 [https]
ADIPOSE TISSUE MACROPHAGES
INMUNOMETABOLISM
Medicina Básica
Phenotype
Adipose Tissue
Oncology
OBESITY
Immunology and Microbiology Section
purl.org/becyt/ford/3 [https]
adipose tissue macrophages
medicine.medical_specialty
CIENCIAS MÉDICAS Y DE LA SALUD
Trypanosoma cruzi
Adipose tissue macrophages
Inmunología
Macrophage polarization
Biology
Diet
High-Fat

Diabetes Mellitus
Experimental

03 medical and health sciences
Immune system
Insulin resistance
Internal medicine
Diabetes mellitus
medicine
Animals
Chagas Disease
Immune response
Macrophages
Immunity
nutritional and metabolic diseases
medicine.disease
Fatty Liver
Mice
Inbred C57BL

Disease Models
Animal

Chronic infection
030104 developmental biology
Endocrinology
Chronic Disease
Immunology
INNATE IMMUNITY
Insulin Resistance
Steatosis
Zdroj: CONICET Digital (CONICET)
Consejo Nacional de Investigaciones Científicas y Técnicas
instacron:CONICET
Oncotarget
ISSN: 1949-2553
Popis: Chronic 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, suggesting the presence of pro-atherogenic small and dense LDL particles. Moreover, acute insulin resistance followed by chronic hyperglycemia with hypoinsulinemia was found, evidencing an infection-related-diabetes progression. These lipid and glucose metabolic changes seemed to be highly dependent on TLR4 expression since TLR4-/- mice were protected from obesity and its complications. Notably, chronic infection promoted a strong increase in MCP-1 producing macrophages with a M2 (F4/80+CD11c-CD206+) phenotype associated to oxidative stress in visceral adipose tissue of DIO+I mice. Importantly, infection reduced lipid content but intensified inflammatory infiltrates in target tissues. Thus, parasite persistence in an obesogenic environment and the resulting host immunometabolic dysregulation may contribute to diabetes/atherosclerosis progression. Fil: Cabalén, María Eugenia. Universidad Católica de Córdoba; Argentina Fil: Cabral, Maria Fernanda. Universidad Católica de Córdoba; Argentina Fil: Sanmarco, Liliana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Andrada, Marta Cecilia. Universidad Católica de Córdoba; Argentina Fil: Onofrio, Luisina Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Ponce, Nicolás Eric. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Aoki, Maria del Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Gea, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Cano, Roxana Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Databáze: OpenAIRE