The Roles of Neutrophils Linking Periodontitis and Atherosclerotic Cardiovascular Diseases

被引:32
|
作者
Irwandi, Rizky A. [1 ]
Chiesa, Scott T. [2 ]
Hajishengallis, George [3 ]
Papayannopoulos, Venizelos [4 ]
Deanfield, John E. [2 ]
D'Aiuto, Francesco [1 ]
机构
[1] UCL, UCL Eastman Dent Inst, Periodontol Unit, London, England
[2] UCL, UCL Inst Cardiovasc Sci, London, England
[3] Univ Penn, Dept Basic & Translat Sci, Lab Innate Immun & Inflammat, Penn Dent Med, Philadelphia, PA USA
[4] Francis Crick Inst, Antimicrobial Def Lab, London, England
来源
FRONTIERS IN IMMUNOLOGY | 2022年 / 13卷
基金
美国国家卫生研究院;
关键词
neutrophils; systemic inflammation; trained immunity; innate immune memory; periodontitis; periodontal disease; atherosclerosis; atherosclerotic cardiovascular disease; PERIPHERAL-BLOOD NEUTROPHILS; ACUTE MYOCARDIAL-INFARCTION; GINGIVAL CREVICULAR FLUID; HEMATOPOIETIC STEM-CELLS; EXTRACELLULAR TRAPS; CYTOKINE PRODUCTION; CATHEPSIN-G; PORPHYROMONAS-GINGIVALIS; ENDOTHELIAL DYSFUNCTION; GLOBAL BURDEN;
D O I
10.3389/fimmu.2022.915081
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammation plays a crucial role in the onset and development of atherosclerosis. Periodontitis is a common chronic disease linked to other chronic inflammatory diseases such as atherosclerotic cardiovascular disease (ASCVD). The mechanistic pathways underlying this association are yet to be fully understood. This critical review aims at discuss the role of neutrophils in mediating the relationship between periodontitis and ASCVD. Systemic inflammation triggered by periodontitis could lead to adaptations in hematopoietic stem and progenitor cells (HSPCs) resulting in trained granulopoiesis in the bone marrow, thereby increasing the production of neutrophils and driving the hyper-responsiveness of these abundant innate-immune cells. These alterations may contribute to the onset, progression, and complications of atherosclerosis. Despite the emerging evidence suggesting that the treatment of periodontitis improves surrogate markers of cardiovascular disease, the resolution of periodontitis may not necessarily reverse neutrophil hyper-responsiveness since the hyper-inflammatory re-programming of granulopoiesis can persist long after the inflammatory inducers are removed. Novel and targeted approaches to manipulate neutrophil numbers and functions are warranted within the context of the treatment of periodontitis and also to mitigate its potential impact on ASCVD.
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收藏
页数:15
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