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• W4285370334 abstract "Psychological stress is associated with elevated circulating markers of inflammation, including inflammatory cytokines and acute phase reactants that accelerate progression of chronic inflammatory diseases (e.g., atherosclerosis, metabolic syndrome, autoimmune diseases and cancer). However, the mechanisms underlying inflammatory reactivity to stress and how it confers future health risk are poorly understood. Monocyte-derived macrophages play key roles in sustaining tissue inflammation, and recent studies show that they can maintain epigenetic memory of pathogen or sterile inflammatory insults, leading to a heightened inflammatory state upon secondary stimulation. We show herein that psychological stress induces transcriptomic and epigenomic reprogramming of monocytes which primes them for a heightened inflammatory immune response following challenge. Monocytes isolated from stressed mice or humans with high reported levels of psychological stress exhibit a common signature of heightened inflammatory gene expression and produce increased levels of proinflammatory cytokines upon ex vivo stimulation with Toll-like receptor ligands. RNA and ATAC sequencing studies revealed that monocytes from stressed mice and humans exhibit activation of cellular metabolic pathways, including mTOR and PI3Kinase pathways, and reduced chromatin accessibility at loci associated with mitochondrial respiration. Taken together, our findings suggest that psychological stress primes the reprogramming of innate immune cells resulting in a hyperresponsive inflammatory state, which may explain its deleterious association with inflammatory disease risk." @default.
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• W4285370334 date "2021-09-01" @default.
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• W4285370334 title "Abstract 105: Chronic Stress Primes Innate Immune Responses In Mice And Humans" @default.
• W4285370334 doi "https://doi.org/10.1161/atvb.41.suppl_1.105" @default.
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