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- W4313374583 startingPage "70.18" @default.
- W4313374583 abstract "Abstract Influenza infection (Flu) is a cause of morbidity and mortality that poses increased risk to children and lacks consistent treatment. Modulating immunometabolism has therapeutic potential. Immune metabolism in response to TLR agonists is well characterized compared to Flu. Clinical reports indicate Flu induces hypermetabolism in the lungs and draining lymph nodes. We demonstrated epithelial cells may be a contributing factor as Flu significantly increased glycolysis, glucose uptake, and lactate excretion and reports suggest these conditions diminish immune function. Dendritic cells (DC) and macrophages (MO) are thought to have rigid metabolic profiles that dictate inflammatory phenotypes after TLR stimulation. We found during Flu epithelial cells, DC, and MO have similar metabolism through shared and distinct molecular mechanisms that allow innate cells to retain metabolic plasticity. We found DC and MO significantly increase both glycolysis and respiration in response to Flu while TLR agonists induce glycolysis with respiratory defects. DC from murine lungs during Flu had the same metabolic phenotype. However, when DC metabolism was constrained motility and T cell priming were diminished. We identified a metabolic drug that significantly improved infection outcomes in vivo and reduced Flu in a clinical trial. Its antiviral mechanism is unknown, but we found it cell specifically modulates metabolic regulators and effector function. To investigate this in humans we collected upper airway cells and secretions from children with respiratory viral infections and found glycolysis and respiration were significantly increased. Thus, we find Flu induces hypermetabolism in vitro, in vivo, and in children’s respiratory tract." @default.
- W4313374583 created "2023-01-06" @default.
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- W4313374583 date "2020-05-01" @default.
- W4313374583 modified "2023-09-27" @default.
- W4313374583 title "Dynamic metabolic reprogramming in innate immune cells: an early response to influenza infection that is essential for effector function" @default.
- W4313374583 doi "https://doi.org/10.4049/jimmunol.204.supp.70.18" @default.
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