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 |
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| 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 |
| DOI: | 10.18632/oncotarget.7630 |
| 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 |
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