Trained innate immunity and atherosclerosis

被引:51
作者
Bekkering, Siroon [1 ,2 ]
Joosten, Leo A. B. [1 ,2 ]
van der Meer, Jos W. M. [1 ,2 ]
Netea, Mihai G. [1 ,2 ]
Riksen, Niels P. [3 ]
机构
[1] Radboud Univ Nijmegen, Med Ctr, Dept Internal Med, Div Expt Med, NL-6500 HB Nijmegen, Netherlands
[2] Nijmegen Inst Infect Inflammat & Immun N4i, Nijmegen, Netherlands
[3] Radboud Univ Nijmegen, Med Ctr, Dept Internal Med, Div Vasc Med, NL-6500 HB Nijmegen, Netherlands
关键词
atherosclerosis; epigenetic modification; inflammation; innate immunity; LOW-DENSITY-LIPOPROTEIN; MEDIATED HISTONE MODIFICATIONS; CHLAMYDIA-PNEUMONIAE; CANDIDA-ALBICANS; GENE-EXPRESSION; INFECTIOUS BURDEN; DNA METHYLATION; EPIGENETICS; MICE; INFLAMMATION;
D O I
10.1097/MOL.0000000000000023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Purpose of reviewMonocytes/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 findingsRecently, 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-Guerin, 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.SummaryWe 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.
引用
收藏
页码:487 / 492
页数:6
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