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- W4313382018 abstract "Abstract Macrophages (mϕ) act as one of the prime barriers to Trypanosoma cruzi infection yet fail to achieve complete clearance of the parasite. The phenotypic diversity of mϕ include pro-inflammatory and immunomodulatory activated states which are supported by cytosolic glycolysis and mitochondrial oxidative phosphorylation (OXPHOS), respectively, for their differential functions. We previously reported that murine mϕ (RAW264.7 or bone marrow-derived) infected with T. cruzi Sylvio strain (SYL) produce TNF-α, but low levels of reactive oxygen species (ROS) and nitric oxide (NO) and fail to switch to the glycolysis observed in the pro-inflammatory LPS/IFNG-induced mϕ. Pre-blockage of OXPHOS with the ATP synthase inhibitor, oligomycin, resulted in further suppression of NO in mϕ responding to SYL. These data suggested that SYL-infected mϕ may utilize mitochondrial metabolism as an initial activator of NO production. Providing interferon-γ (IFNG) during SYL infection of mϕ shut down OXPHOS and produced ROS and NO as observed in pro-inflammatory controls by 18 hours posttreatment. We hypothesized that glycolysis was required for the activation of IFNG/SYL- and LPS/IFNG-induced ROS and NO in mϕ. We found that eliminating glucose from the culture media or inhibiting glucose uptake resulted in the failure of ROS and NO production, but sustained TNF-α release. The protein expression of the ROS-producing NADPH oxidase (NOX2) subunit, gp91phox, was not detected in SYL-infected mϕ although abundant in pro-inflammatory mϕ. These data suggest that glycolysis may regulate NOX2 activation in mϕ responding to inflammatory stimuli. How NOX2 function and NO release is controlled by glucose and mitochondrial metabolism in mϕ will be further discussed." @default.
- W4313382018 created "2023-01-06" @default.
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- W4313382018 date "2017-05-01" @default.
- W4313382018 modified "2023-09-27" @default.
- W4313382018 title "Glucose metabolism regulates reactive oxygen species and nitric oxide production of macrophages in response to IFN-γ and <i>Trypanosoma cruzi</i>" @default.
- W4313382018 doi "https://doi.org/10.4049/jimmunol.198.supp.216.6" @default.
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