免疫
免疫学
免疫系统
炎症
重编程
医学
先天免疫系统
表观遗传学
促炎细胞因子
骨髓
骨髓生成
髓样
生物
离体
免疫调节
祖细胞
获得性免疫系统
全身炎症
髓系细胞
细胞免疫
斯达
细胞因子
干细胞
造血
体内
作者
Niels P. Riksen,Quirijn de Mast
标识
DOI:10.1161/atvbaha.125.322608
摘要
Innate immune cells can develop a long-lasting hyperresponsive phenotype by metabolic and epigenetic reprogramming after brief exposure to inflammatory stimuli. Several experimental studies convincingly demonstrated that this immunologic phenomenon, which is called trained immunity, can accelerate the development of atherosclerosis. In this brief review, we summarize current evidence that diets and specific dietary components can modulate trained immunity. In mice, intermittent high-fat diets can reprogram bone marrow myeloid progenitor cells, resulting in hyperinflammatory monocytes and neutrophils that aggravate atherosclerosis. Diet-induced obesity also leads to persistent proinflammatory epigenetic reprogramming of myeloid cells and adipocytes. Hyperglycemia and high-salt diets can also induce trained immunity in murine models. Recent intervention studies in Tanzania revealed that urban Western-style diets trigger systemic inflammation and immune activation, whereas a traditional plant-based heritage diet limits inflammation. Ex vivo studies suggest that this is caused, at least in part, by modulation of trained immunity. Various individual dietary components, such as the flavone apigenin and the polyphenol resveratrol, are able to prevent trained immunity in vitro. It is exciting to speculate how further molecular elucidation on the modulation of trained immunity by diets or isolated dietary components could help to prevent cardiovascular diseases.
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