scholarly journals The Effects of Porphyromonas gingivalis on Atherosclerosis-Related Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiaqi Zhang ◽  
Mengru Xie ◽  
Xiaofei Huang ◽  
Guangjin Chen ◽  
Ying Yin ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Chronic Inflammatory Disease ◽  
Fibrous Materials ◽  
Periodontal Pathogens ◽  
T Helper ◽  
Specific Mechanism ◽  
Infective Disease ◽  
New Perspective ◽  
Underlying Mechanisms ◽  
Progression Of Atherosclerosis

Atherosclerosis (AS), one of the most common types of cardiovascular disease, has initially been attributed to the accumulation of fats and fibrous materials. However, more and more researchers regarded it as a chronic inflammatory disease nowadays. Infective disease, such as periodontitis, is related to the risk of atherosclerosis. Porphyromonas gingivalis (P. gingivalis), one of the most common bacteria in stomatology, is usually discovered in atherosclerotic plaque in patients. Furthermore, it was reported that P. gingivalis can promote the progression of atherosclerosis. Elucidating the underlying mechanisms of P. gingivalis in atherosclerosis attracted attention, which is thought to be crucial to the therapy of atherosclerosis. Nevertheless, the pathogenesis of atherosclerosis is much complicated, and many kinds of cells participate in it. By summarizing existing studies, we find that P. gingivalis can influence the function of many cells in atherosclerosis. It can induce the dysfunction of endothelium, promote the formation of foam cells as well as the proliferation and calcification of vascular smooth muscle cells, and lead to the imbalance of regulatory T cells (Tregs) and T helper (Th) cells, ultimately promoting the occurrence and development of atherosclerosis. This article summarizes the specific mechanism of atherosclerosis caused by P. gingivalis. It sorts out the interaction between P. gingivalis and AS-related cells, which provides a new perspective for us to prevent or slow down the occurrence and development of AS by inhibiting periodontal pathogens.

scholarly journals Porphyromonas gingivalis and its impact on periodontal health and systemic diseases. A concise review.

2019 ◽  
Vol 6 (1) ◽  
pp. 31-34
Author(s):  
Pablo Jasma ◽  
Patricio Sánchez
Keyword(s):  
Porphyromonas Gingivalis ◽  
Vascular Inflammation ◽  
Bacterial Species ◽  
Low Frequency ◽  
Chronic Inflammatory Disease ◽  
Periodontal Pathogens ◽  
Periodontal Health ◽  
Concise Review ◽  
Cardiovascular Cells ◽  
Systemic Health

Periodontitis is defined as a multifactorial chronic inflammatory disease, associated to a dysbiotic biofilm and characterized by the progressive destruction of the periodontal attachment. Clinical studies have revealed the presence of 10 to 15 bacterial species that are potential periodontal pathogens in adults. From these, the most cited are Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Tannerella forsythia. The aim of this article is to review P. gingivalis’ characteristics and impact on periodontal and systemic health. Different studies have reported a relation between the presence of P. gingivalis and periodontal disease. P. gingivalis was one of the most frequently detected species in aggressive and chronic periodontitis. This is due to its unique ability to avoid the host’s immune response and contribute to the development of the destructive process. P. gingivalis, although only present in low frequency, is pathogenic because of its ability to induce dysbiotic microbial communities. There is more evidence that P. gingivalis might invade cardiovascular cells and tissues causing inflammation. It has been suggested that NLRP3 inflammasome plays a key role in the development of vascular inflammation and atherosclerosis. The repeated exposure to P. gingivalis, produces neuroinflammation, neurodegeneration and formation of intra and extracellular amyloid plaques, which are pathognomonic signs of Alzheimer’s disease.

scholarly journals Association between Green Space Structure and the Prevalence of Asthma: A Case Study of Toronto

2021 ◽  
Vol 18 (11) ◽  
pp. 5852
Author(s):  
Yuping Dong ◽  
Helin Liu ◽  
Tianming Zheng
Keyword(s):  
Air Pollution ◽  
Vegetation Index ◽  
Green Space ◽  
Normalized Difference Vegetation Index ◽  
Chronic Inflammatory Disease ◽  
Space Structure ◽  
Tree Diversity ◽  
Underlying Mechanisms ◽  
Index Tree

Asthma is a chronic inflammatory disease that can be caused by various factors, such as asthma-related genes, lifestyle, and air pollution, and it can result in adverse impacts on asthmatics’ mental health and quality of life. Hence, asthma issues have been widely studied, mainly from demographic, socioeconomic, and genetic perspectives. Although it is becoming increasingly clear that asthma is likely influenced by green spaces, the underlying mechanisms are still unclear and inconsistent. Moreover, green space influences the prevalence of asthma concurrently in multiple ways, but most existing studies have explored only one pathway or a partial pathway, rather than the multi-pathways. Compared to greenness (measured by Normalized Difference Vegetation Index, tree density, etc.), green space structure—which has the potential to impact the concentration of air pollution and microbial diversity—is still less investigated in studies on the influence of green space on asthma. Given this research gap, this research took Toronto, Canada, as a case study to explore the two pathways between green space structure and the prevalence of asthma based on controlling the related covariates. Using regression analysis, it was found that green space structure can protect those aged 0–19 years from a high risk of developing asthma, and this direct protective effect can be enhanced by high tree diversity. For adults, green space structure does not influence the prevalence of asthma unless moderated by tree diversity (a measurement of the richness and diversity of trees). However, this impact was not found in adult females. Moreover, the hypothesis that green space structure influences the prevalence of asthma by reducing air pollution was not confirmed in this study, which can be attributed to a variety of causes.

scholarly journals In Situ Anabolic Activity of Periodontal Pathogens Porphyromonas gingivalis and Filifactor alocis in Chronic Periodontitis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Ralee Spooner ◽  
Kris M. Weigel ◽  
Peter L. Harrison ◽  
KyuLim Lee ◽  
Gerard A. Cangelosi ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Chronic Periodontitis ◽  
Periodontal Pathogens ◽  
Anabolic Activity ◽  
Filifactor Alocis

scholarly journals The Protective Role of Sestrin2 in Atherosclerotic and Cardiac Diseases

2021 ◽  
Vol 22 (3) ◽  
pp. 1200
Author(s):  
Yoshimi Kishimoto ◽  
Kazuo Kondo ◽  
Yukihiko Momiyama
Keyword(s):  
Oxidative Stress ◽  
Protective Role ◽  
Chronic Inflammatory Disease ◽  
Atherosclerotic Disease ◽  
Cardiac Diseases ◽  
Compensatory Response ◽  
Age Related ◽  
Anti Oxidant ◽  
Progression Of Atherosclerosis

Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases.

scholarly journals Porphyromonas gingivalis oral infection promote T helper 17/Treg imbalance in the development of atherosclerosis

2017 ◽  
Vol 12 (1) ◽  
pp. 60-69 ◽  
Author(s):  
Jie Yang ◽  
Juan Wu ◽  
Rui Zhang ◽  
Min Yao ◽  
Yu Liu ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Oral Infection ◽  
T Helper ◽  
T Helper 17

scholarly journals Borrelia burgdorferi activates a T helper type 1-like T cell subset in Lyme arthritis.

1991 ◽  
Vol 174 (3) ◽  
pp. 593-601 ◽  
Author(s):  
H Yssel ◽  
M C Shanafelt ◽  
C Soderberg ◽  
P V Schneider ◽  
J Anzola ◽  
...  
Keyword(s):  
T Cell ◽  
Borrelia Burgdorferi ◽  
Cell Subset ◽  
Chronic Inflammatory Disease ◽  
T Cell Response ◽  
Lyme Arthritis ◽  
T Helper ◽  
Cell Clones ◽  
T Cell Lines

18 cloned T cell lines reactive with Borrelia burgdorferi proteins, all CD3+4+8-TCR-alpha/beta+ and restricted by HLA class II proteins, were isolated from four patients with chronic Lyme arthritis. Analysis of these T cell clones indicated that the T cell response to the Lyme disease spirochete is not oligoclonally restricted; yet all produced the same pattern of lymphokines, resembling that of murine type 1 T helper cells, after antigen-specific or nonspecific stimulation. Therefore, a subset of human CD4+ T cells, with a distinct profile of lymphokine secretion, is selectively activated by the pathogen inciting this chronic inflammatory disease.

scholarly journals The link between the genetic polymorphisms of the innate immune signaling molecular factors with periodontitis

2018 ◽  
Vol 91 (1) ◽  
Author(s):  
Gurumoorthy Kaarthikeyan ◽  
Anandan Balakrishnan ◽  
Nadathur Doraisamy Jayakumar
Keyword(s):  
Genetic Polymorphisms ◽  
Chronic Inflammatory Disease ◽  
Innate Immune ◽  
Periodontal Pathogens ◽  
First Line ◽  
Immune Signaling ◽  
Multiple Risk Factors ◽  
Innate Immune Signaling ◽  
Innate Immune Mechanism ◽  
Periodontal Destruction

Periodontitis is a chronic inflammatory disease causing destruction of supporting tissues of teeth. Even though the gramnegative anaerobes are essential for the initiation of periodontal destruction, multiple risk factors are essential for the progression of the disease. The genetic risk factor plays a significant role in the etiopathogenesis of periodontal disease. The innate immune mechanism is the first line of defense in screening and combating the invading periodontal pathogens. The genetic polymorphisms in the 3’UTR region of the innate immune signaling molecular factors like toll-like receptors, nod-like receptors and the polymorphisms in the epigenetic regulators of these factors like microRNA146a, apolipoproteinE might play an important role in the etiopathogenesis of periodontal destruction.

MicroRNAs in the regulation of immune cell functions – implications for atherosclerotic vascular disease

2012 ◽  
Vol 107 (04) ◽  
pp. 626-633 ◽  
Author(s):  
Alma Zernecke
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Molecular Mechanisms ◽  
Immune Cell ◽  
Chronic Inflammatory Disease ◽  
Vascular Pathology ◽  
Lipid Uptake ◽  
T Helper ◽  
Atherosclerotic Vascular Disease ◽  
Cell Functions

SummaryRegarded as a chronic inflammatory disease of the vessel wall, the development of atherosclerotic lesions is shaped by immune responses and their regulation. Macrophages and dendritic cells are positioned at the crossroad of innate and adaptive immune responses by sensing atherogenic danger signals and by taking up and presenting antigens. T helper cells and auto-antibodies produced by B cells, together with their cytokine responses in turn modulate atheroprogression. In addition, platelets contribute to atherosclerosis by multiple pathways. microRNAs (miRNAs) that post-transcriptionally regulate gene expression may thus critically control immune cell differentiation and functions during plaque evolution. This review summarises the role of miRNAs in regulating lipid uptake and expression of inflammatory mediators in monocytes/macrophages and dendritic cells, in lymphocyte functions with a focus on T helper cell responses, as well as in platelet biology, and the implications of altering these functions in vascular pathology and atherosclerosis. T systematically survey miRNA functions in controlling molecular mechanisms and immune responses in atherosclerosis holds potential for the development of novel miRNA-based strategies for therapies targeting inflammation and immunity in atherosclerosis.

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