ArticleInfection and immunity2016
Macrophages Promote Oxidative Metabolism To Drive Nitric Oxide Generation in Response to Trypanosoma cruzi.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Comparative 5' IsomiRome Analysis Uncovers Dysregulated 5' IsomiRs inComputational and structural biotechnology journal · 2026Article
- Trypanosoma Cruzi Lineages Shape Macrophage Cytokine Profiles in Single and Mixed Infections.Parasite immunology · 2025Article
- Differential antioxidant enzyme profiles reveal early molecular signatures of virulence inFrontiers in cellular and infection microbiology · 2025Article
- Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease.PLoS pathogens · 2024Review
- Metabolism and immune responses of striped hamsters to ectoparasite challenges: insights from transcriptomic analysis.Frontiers in immunology · 2024Article
- From Benznidazole to New Drugs: Nanotechnology Contribution in Chagas Disease.International journal of molecular sciences · 2023Review
- Macrophage Polarization Status Impacts Nanoceria Cellular Distribution but Not Its Biotransformation or Ferritin Effects.Nanomaterials (Basel, Switzerland) · 2023Article
- Cardiomyocyte infection byFrontiers in cellular and infection microbiology · 2023Article
- Article
- Platelets, Macrophages, and Thromboinflammation in Chagas Disease.Journal of inflammation research · 2022Review
- Oxidative stress implications for therapeutic vaccine development against Chagas disease.Expert review of vaccines · 2021Review
- Central role of metabolism in Trypanosoma cruzi tropism and Chagas disease pathogenesis.Current opinion in microbiology · 2021Review
- Absence of Bim sensitizes mice to experimental Trypanosoma cruzi infection.Cell death & disease · 2021Article
- Non-Invasive Differentiation of M1 and M2 Activation in Macrophages Using HyperpolarizedMetabolites · 2021Article
- Lymphotoxin β Receptor: a Crucial Role in Innate and Adaptive Immune Responses against Toxoplasma gondii.Infection and immunity · 2021Article
- Human NK cells: From development to effector functions.Innate immunity · 2021Review
- DNA damage and oxidative stress in human cells infected by Trypanosoma cruzi.PLoS pathogens · 2021Article
- Sirtuin Control of Mitochondrial Dysfunction, Oxidative Stress, and Inflammation in Chagas Disease Models.Frontiers in cellular and infection microbiology · 2021Review
- The Oxidative Stress and Chronic Inflammatory Process in Chagas Disease: Role of Exosomes and Contributing Genetic Factors.Oxidative medicine and cellular longevity · 2021Review
- Co-Exposure of Cardiomyocytes to IFN-γ and TNF-α Induces Mitochondrial Dysfunction and Nitro-Oxidative Stress: Implications for the Pathogenesis of Chronic Chagas Disease Cardiomyopathy.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Trypanosoma cruzi is the causative agent of chronic chagasic cardiomyopathy. Why macrophages (mφs), the early responders to infection, fail to achieve parasite clearance is not known. Mouse (RAW 264.7) and human (THP-1 and primary) mφs were infected for 3 h and 18 h with T. cruzi TcI isolates, SylvioX10/4 (SYL, virulent) and TCC (nonpathogenic), which represent mφ stimulation and infection states, respectively. Mφs incubated with lipopolysaccharide and gamma interferon (LPS/IFN-γ) and with interleukin-4 (IL-4) were used as controls. We monitored the cytokine profile (using enzyme-linked immunosorbent assay [ELISA]), reactive oxygen species (ROS; fluorescent probes), nitric oxide (·NO; Griess assay), and metabolic state using a custom-designed mitoxosome array and Seahorse XF24 Analyzer. LPS/IFN-γ treatment of mφs elicited a potent increase in production of tumor necrosis alpha (TNF-α) at 3 h and of ROS and ·NO by 18 h. Upon SYL infection, murine mφs elicited an inflammatory cytokine profile (TNF-α ≫ TGF-β + IL-10) and low levels of ·NO and ROS production. LPS/IFN-γ treatment resulted in the inhibition of oxidative metabolism at the gene expression and functional levels and a switch to the glycolytic pathway in mφs, while IL-4-treated mφs utilized oxidative metabolism to meet energy demands. SYL infection resulted in an intermediate functional metabolic state with increased mitoxosome gene expression and glycolysis, and IFN-γ addition shut down the oxidative metabolism in SYL-infected mφs. Further, TCC- and SYL-stimulated mφs exhibited similar levels of cell proliferation and production of TNF-α and ROS, while TCC-stimulated mφs exhibited up to 2-fold-higher levels of oxidative metabolism and ·NO production than SYL-infected mφs. Inhibiting ATP-coupled O
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