Siroon Bekkering1, Leo A B Joosten, Jos W M van der Meer, Mihai G Netea, Niels P Riksen. 1. aDepartment of Internal Medicine, Division of Experimental Medicine, Radboud University Nijmegen Medical Centre bNijmegen Institute for Infection, Inflammation and Immunity (N4i) cDepartment of Internal Medicine, Division of Vascular Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Abstract
PURPOSE OF REVIEW: Monocytes/macrophages play a decisive role in the development and progression of atherosclerosis. It is currently unknown what stimuli initiate and orchestrate the activation of these cells in atherogenesis. In this review, we postulate that the novel concept of 'trained immunity' modulates the development and progression of atherosclerosis. RECENT FINDINGS: Recently, results from our laboratory challenged the current paradigm that innate immunity is static and does not have an immunological memory. Stimulation by various microbial products, including Candida albicans and bacille Calmette-Guérin, appeared to bring monocytes into a long-term enhanced functional state, showing a stronger proinflammatory response to a second stimulus. This 'trained immunity' was mediated by increased and stable histone methylation. SUMMARY: We describe the hypothesis that this functional reprogramming of monocytes, either by microbial products or by metabolic products, contributes to atherogenesis and propose epigenetic reprogramming of monocytes as a novel pharmacological target for preventing or treating atherosclerosis in the future.
PURPOSE OF REVIEW: Monocytes/macrophages play a decisive role in the development and progression of atherosclerosis. It is currently unknown what stimuli initiate and orchestrate the activation of these cells in atherogenesis. In this review, we postulate that the novel concept of 'trained immunity' modulates the development and progression of atherosclerosis. RECENT FINDINGS: Recently, results from our laboratory challenged the current paradigm that innate immunity is static and does not have an immunological memory. Stimulation by various microbial products, including Candida albicans and bacille Calmette-Guérin, appeared to bring monocytes into a long-term enhanced functional state, showing a stronger proinflammatory response to a second stimulus. This 'trained immunity' was mediated by increased and stable histone methylation. SUMMARY: We describe the hypothesis that this functional reprogramming of monocytes, either by microbial products or by metabolic products, contributes to atherogenesis and propose epigenetic reprogramming of monocytes as a novel pharmacological target for preventing or treating atherosclerosis in the future.
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