ArticleOncotarget2016
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.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Interplay of obesity and parasitic infection: current evidence of immunogenesis, tumorigenesis and leptin receptor involvement.Nutrition & metabolism · 2025Review
- A novel mouse model for studying complications related to type 2 diabetes using a medium-fat diet, fructose, and streptozotocin.Scientific reports · 2025Article
- Adipose Tissue in Chagas Disease: A Neglected Component of Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- Anti-Inflammatory Effects of Helminth-Derived Products: Potential Applications and Challenges in Diabetes Mellitus Management.Journal of inflammation research · 2024Review
- Interaction between peripheral blood mononuclear cells andFrontiers in immunology · 2024Article
- Benznidazole treatment decreases IL-6 levels in Trypanosoma cruzi-infected human adipocytes differentiated from adipose tissue-derived stem cells.Memorias do Instituto Oswaldo Cruz · 2023Article
- Comorbidities involving parasitic diseases: A look at the benefits and complications.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Immune and non-immune functions of adipose tissue leukocytes.Nature reviews. Immunology · 2022Review
- Helminth and Host Crosstalk: New Insight Into Treatment of Obesity and Its Associated Metabolic Syndromes.Frontiers in immunology · 2022Review
- Trypanosoma brucei triggers a broad immune response in the adipose tissue.PLoS pathogens · 2021Article
- Infections at the nexus of metabolic-associated fatty liver disease.Archives of toxicology · 2021Review
- Review
- Diet Rich in Lard Promotes a Metabolic Environment Favorable toFrontiers in cardiovascular medicine · 2021Article
- The role of fat on cardiomyopathy outcome in mouse models of chronic Trypanosoma cruzi infection.Parasitology research · 2020Article
- Myocardial Involvement in Chagas Disease and Insulin Resistance: A Non-Metabolic Model of Cardiomyopathy.Global heart · 2020Article
- Genes of the cGMP-PKG-CaBiochimica et biophysica acta. Molecular basis of disease · 2020Article
- Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice.Scientific reports · 2019Article
- Hemozoin-induced activation of human monocytes toward M2-like phenotype is partially reversed by antimalarial drugs-chloroquine and artemisinin.MicrobiologyOpen · 2019Article
- Advances in understanding the role of adipose tissue and mitochondrial oxidative stress inF1000Research · 2019Review
- Role of Hormonal Circuitry Upon T Cell Development in Chagas Disease: Possible Implications on T Cell Dysfunctions.Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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