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牙龈卟啉单胞菌与树突状细胞的相互作用:对冠状动脉疾病的影响。

Porphyromonas gingivalis-dendritic cell interactions: consequences for coronary artery disease.

机构信息

Department of Molecular Genetics and Microbiology, Center for Infectious Diseases, Stony Brook University, Stony Brook, NY, USA.

出版信息

J Oral Microbiol. 2010 Dec 21;2. doi: 10.3402/jom.v2i0.5782.

DOI:10.3402/jom.v2i0.5782
PMID:21523219
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3084565/
Abstract

An estimated 80 million US adults have one or more types of cardiovascular diseases. Atherosclerosis is the single most important contributor to cardiovascular diseases; however, only 50% of atherosclerosis patients have currently identified risk factors. Chronic periodontitis, a common inflammatory disease, is linked to an increased cardiovascular risk. Dendritic cells (DCs) are potent antigen presenting cells that infiltrate arterial walls and may destabilize atherosclerotic plaques in cardiovascular disease. While the source of these DCs in atherosclerotic plaques is presently unclear, we propose that dermal DCs from peripheral inflamed sites such as CP tissues are a potential source. This review will examine the role of the opportunistic oral pathogen Porphyromonas gingivalis in invading DCs and stimulating their mobilization and misdirection through the bloodstream. Based on our published observations, combined with some new data, as well as a focused review of the literature we will propose a model for how P. gingivalis may exploit DCs to gain access to systemic circulation and contribute to coronary artery disease. Our published evidence supports a significant role for P. gingivalis in subverting normal DC function, promoting a semimature, highly migratory, and immunosuppressive DC phenotype that contributes to the inflammatory development of atherosclerosis and, eventually, plaque rupture.

摘要

估计有 8000 万美国成年人患有一种或多种心血管疾病。动脉粥样硬化是心血管疾病最重要的单一因素;然而,只有 50%的动脉粥样硬化患者有目前确定的风险因素。慢性牙周炎是一种常见的炎症性疾病,与心血管风险增加有关。树突状细胞(DCs)是浸润动脉壁并可能使心血管疾病中动脉粥样硬化斑块不稳定的有效抗原呈递细胞。虽然目前尚不清楚这些 DCs 在动脉粥样硬化斑块中的来源,但我们提出,来自外周炎症部位(如 CP 组织)的皮肤 DC 可能是一个潜在的来源。这篇综述将探讨机会性病原体牙龈卟啉单胞菌(Porphyromonas gingivalis)入侵 DCs 并通过血液刺激其动员和错误定向的作用。基于我们已发表的观察结果,结合一些新的数据,以及对文献的重点回顾,我们将提出一个模型,说明 P. gingivalis 如何利用 DCs 进入全身循环并导致冠状动脉疾病。我们已发表的证据表明,P. gingivalis 在破坏正常 DC 功能方面起着重要作用,促进了一种半成熟、高迁移性和免疫抑制性的 DC 表型,这有助于动脉粥样硬化的炎症发展,并最终导致斑块破裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a93/3084565/05b3ad97da04/JOM-2-5782-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a93/3084565/05b3ad97da04/JOM-2-5782-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a93/3084565/05b3ad97da04/JOM-2-5782-g001.jpg

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本文引用的文献

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The native 67-kilodalton minor fimbria of Porphyromonas gingivalis is a novel glycoprotein with DC-SIGN-targeting motifs.牙龈卟啉单胞菌天然 67 千道尔顿小菌毛是一种具有 DC-SIGN 靶向基序的新型糖蛋白。
J Bacteriol. 2010 Aug;192(16):4103-10. doi: 10.1128/JB.00275-10. Epub 2010 Jun 18.
2
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Nat Rev Microbiol. 2010 Jul;8(7):481-90. doi: 10.1038/nrmicro2337.
3
Chemokines and their receptors in the allergic airway inflammatory process.趋化因子及其受体在过敏性气道炎症过程中的作用。
与系统性疾病的关联:聚焦 T 细胞介导的适应性免疫。
Front Cell Infect Microbiol. 2022 Nov 17;12:1026457. doi: 10.3389/fcimb.2022.1026457. eCollection 2022.
4
Interleukin-34 permits Porphyromonas gingivalis survival and NF-κB p65 inhibition in macrophages.白细胞介素-34 可使牙龈卟啉单胞菌在巨噬细胞中存活并抑制 NF-κB p65。
Mol Oral Microbiol. 2022 Jun;37(3):109-121. doi: 10.1111/omi.12366. Epub 2022 May 27.
5
The Effects of on Atherosclerosis-Related Cells.对动脉粥样硬化相关细胞的影响。
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6
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Clin Immunol. 2010 Jan;134(1):25-32. doi: 10.1016/j.clim.2009.05.006. Epub 2009 Jun 10.