Abstract
Abstract Macrophage activation rely on the metabolism which supports the generation of compounds crucial for proper cell function. Aerobic metabolism is dependent on mitochondrial oxidative phosphorylation, and is essential for the activation of immunomodulatory macrophages (M2). Conversely, mitochondria-independent, anaerobic metabolism provides substrates to produce anti-microbial mediators by pro-inflammatory macrophages (M1). Reactive oxygen species (ROS) and nitric oxide (NO) are key M1 molecules for host defense against intracellular parasites, including the etiologic agent of Chagas disease, Trypanosoma cruzi. In this study, we report deficient production of ROS and NO by macrophages infected with T. cruzi (H2DCFDA, Amplex Red and Griess assays), and show that mitochondrial gene expression (qPCR) and function (Seahorse Extracellular Flux Analyzer) are in concordance with the M2 phenotype and macrophage susceptibility to T. cruzi infection. These findings indicate the possibility of manipulating oxygen metabolism to improve the pro-inflammatory function and pathogen clearance by macrophages.
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