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Porphyromonas gingivalis regulates atherosclerosis through an immune pathway

Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several i...

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Autores principales: Ruan, Qijun, Guan, Peng, Qi, Weijuan, Li, Jiatong, Xi, Mengying, Xiao, Limin, Zhong, Sulan, Ma, Dandan, Ni, Jia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10043234/
https://www.ncbi.nlm.nih.gov/pubmed/36999040
http://dx.doi.org/10.3389/fimmu.2023.1103592
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author Ruan, Qijun
Guan, Peng
Qi, Weijuan
Li, Jiatong
Xi, Mengying
Xiao, Limin
Zhong, Sulan
Ma, Dandan
Ni, Jia
author_facet Ruan, Qijun
Guan, Peng
Qi, Weijuan
Li, Jiatong
Xi, Mengying
Xiao, Limin
Zhong, Sulan
Ma, Dandan
Ni, Jia
author_sort Ruan, Qijun
collection PubMed
description Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several inflammatory diseases, among which periodontitis has been shown to increase the risk of AS. Porphyromonas gingivalis (P. gingivalis), presenting in large numbers in subgingival plaque biofilms, is the “dominant flora” in periodontitis, and its multiple virulence factors are important in stimulating host immunity. Therefore, it is significant to elucidate the potential mechanism and association between P. gingivalis and AS to prevent and treat AS. By summarizing the existing studies, we found that P. gingivalis promotes the progression of AS through multiple immune pathways. P. gingivalis can escape host immune clearance and, in various forms, circulate with blood and lymph and colonize arterial vessel walls, directly inducing local inflammation in blood vessels. It also induces the production of systemic inflammatory mediators and autoimmune antibodies, disrupts the serum lipid profile, and thus promotes the progression of AS. In this paper, we summarize the recent evidence (including clinical studies and animal studies) on the correlation between P. gingivalis and AS, and describe the specific immune mechanisms by which P. gingivalis promotes AS progression from three aspects (immune escape, blood circulation, and lymphatic circulation), providing new insights into the prevention and treatment of AS by suppressing periodontal pathogenic bacteria.
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spelling pubmed-100432342023-03-29 Porphyromonas gingivalis regulates atherosclerosis through an immune pathway Ruan, Qijun Guan, Peng Qi, Weijuan Li, Jiatong Xi, Mengying Xiao, Limin Zhong, Sulan Ma, Dandan Ni, Jia Front Immunol Immunology Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several inflammatory diseases, among which periodontitis has been shown to increase the risk of AS. Porphyromonas gingivalis (P. gingivalis), presenting in large numbers in subgingival plaque biofilms, is the “dominant flora” in periodontitis, and its multiple virulence factors are important in stimulating host immunity. Therefore, it is significant to elucidate the potential mechanism and association between P. gingivalis and AS to prevent and treat AS. By summarizing the existing studies, we found that P. gingivalis promotes the progression of AS through multiple immune pathways. P. gingivalis can escape host immune clearance and, in various forms, circulate with blood and lymph and colonize arterial vessel walls, directly inducing local inflammation in blood vessels. It also induces the production of systemic inflammatory mediators and autoimmune antibodies, disrupts the serum lipid profile, and thus promotes the progression of AS. In this paper, we summarize the recent evidence (including clinical studies and animal studies) on the correlation between P. gingivalis and AS, and describe the specific immune mechanisms by which P. gingivalis promotes AS progression from three aspects (immune escape, blood circulation, and lymphatic circulation), providing new insights into the prevention and treatment of AS by suppressing periodontal pathogenic bacteria. Frontiers Media S.A. 2023-03-14 /pmc/articles/PMC10043234/ /pubmed/36999040 http://dx.doi.org/10.3389/fimmu.2023.1103592 Text en Copyright © 2023 Ruan, Guan, Qi, Li, Xi, Xiao, Zhong, Ma and Ni https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Ruan, Qijun
Guan, Peng
Qi, Weijuan
Li, Jiatong
Xi, Mengying
Xiao, Limin
Zhong, Sulan
Ma, Dandan
Ni, Jia
Porphyromonas gingivalis regulates atherosclerosis through an immune pathway
title Porphyromonas gingivalis regulates atherosclerosis through an immune pathway
title_full Porphyromonas gingivalis regulates atherosclerosis through an immune pathway
title_fullStr Porphyromonas gingivalis regulates atherosclerosis through an immune pathway
title_full_unstemmed Porphyromonas gingivalis regulates atherosclerosis through an immune pathway
title_short Porphyromonas gingivalis regulates atherosclerosis through an immune pathway
title_sort porphyromonas gingivalis regulates atherosclerosis through an immune pathway
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10043234/
https://www.ncbi.nlm.nih.gov/pubmed/36999040
http://dx.doi.org/10.3389/fimmu.2023.1103592
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