Effects of Porphyromonas gingivalis lipopolysaccharide on the expression of key genes involved in cholesterol metabolism in macrophages

Liu, Fen; Wang, Yi; Xu, Jing; Liu, Fangqiang; Hu, Rongdang; Deng, Hui

doi:10.5114/aoms.2016.61909

Cited by 28 publications

(25 citation statements)

References 27 publications

(35 reference statements)

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“…It has been reported that lipopolysaccharides from A. actinomycetemcomitans have a synergistic effect with native low‐density lipoproteins in the formation of foam cells . Similar results have been reported for P. gingivalis and its associated LPS …”

Section: Two‐dimensional Cellular Models Used For the Study Of Endothsupporting

confidence: 82%

Two‐dimensional and three‐dimensional models for studying atherosclerosis pathogenesis induced by periodontopathogenic microorganisms

Gualtero

Lafaurie

Fontanilla

2017

Molecular Oral Microbiology

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Epidemiological studies have established a clinical association between periodontal disease and atherosclerosis. Bacteremia and endotoxemia episodes in patients with periodontitis appear to link these two diseases by inducing a body-wide production of cardiovascular markers. The presence of oral bacteria in atherosclerotic lesions in patients with periodontitis suggests that bacteria, or their antigenic components, induce alterations in the endothelium associated with atherosclerosis. Therefore, a causal mechanism explaining the association between both diseases can be constructed using in vitro models. This review presents current experimental approaches based on in vitro cell models used to shed light on the mechanism by which periodontal pathogenic microorganisms, and their antigenic components, induce proatherosclerotic endothelial activity. Monolayer cultures of endothelial vascular or arterial cells have been used to assess periodontal pathogenic bacteria and their antigenic compounds and endothelial activation. However, these models are not capable of reflecting the physiological characteristics of the endothelium inside vascularized tissue. Therefore, the shift from two-dimensional (2D) cellular models toward three-dimensional (3D) models of endothelial cells resembling an environment close to the physiological environment of the endothelial cell within the endothelium is useful for evaluating the physiological relevance of results regarding the endothelial dysfunction induced by periodontopathogens that are currently obtained from 2D models. The use of in vitro 3D cellular models can also be relevant to the search for therapeutic agents for chronic inflammatory diseases such as atherosclerosis. Here, we present some strategies for the assembly of 3D cultures with endothelial cells, which is useful for the study of periodontopathogen-mediated disease.

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Section: Two‐dimensional Cellular Models Used For the Study Of Endothsupporting

confidence: 82%

Two‐dimensional and three‐dimensional models for studying atherosclerosis pathogenesis induced by periodontopathogenic microorganisms

Gualtero

Lafaurie

Fontanilla

2017

Molecular Oral Microbiology

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“…Monocyte-colony stimulating factor 60 , phorbol ester 61 , tumour necrosis factor (TNF) 62 , IL-4 63 and thiazolidinediones 64,65 can also promote CD36 expression in monocyte/macropahges. By contrast, lipopolysaccharide 66 , dexamethasone 60 , interferon 67 , transforming growth factor (TGF)-β1/2 68 , tamoxifen 69 , and HDL 70 inhibit macrophage CD36 expression, whereas statin treatment has been reported to substantially reduce platelet CD36 expression. 71 [H1] The CD36 protein Full-length human CD36 comprises around 472 amino acids and has a predicted molecular mass of 53 kDa.…”

Section: [H2] Transcriptional Regulationmentioning

confidence: 99%

CD36 in chronic kidney disease: novel insights and therapeutic opportunities

et al. 2017

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CD36 (also known as scavenger receptor B2) is a multifunctional receptor that mediates the binding and cellular uptake of long-chain fatty acids, oxidized lipids and phospholipids, advanced oxidation protein products, thrombospondin and advanced glycation end products, and has roles in lipid accumulation, inflammatory signalling, energy reprogramming, apoptosis and kidney fibrosis. Renal CD36 is mainly expressed in tubular epithelial cells, podocytes and mesangial cells, and is markedly upregulated in the setting of chronic kidney disease (CKD). As fatty acids are the preferred energy source for proximal tubule cells, a reduction in fatty acid oxidation in CKD affects kidney lipid metabolism by disrupting the balance between fatty acid synthesis, uptake and consumption. The outcome is intracellular lipid accumulation, which has an important role in the pathogenesis of kidney fibrosis. In experimental models, antagonist blockade or genetic knockout of CD36 prevents kidney injury, suggesting that CD36 could be a novel target for therapy. Here, we discuss the regulation and post-translational modification of CD36, its role in renal pathophysiology and its potential as a biomarker and as a therapeutic target for the prevention of kidney fibrosis.

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“…[89][90][91][92][93] As demonstrated, Pg participates in the CVD progression due to its fixation on the atheroma as LMR. 47,48,50,[94][95][96] These particular anaerobic, cram-negative bacteria can aggregate in red blood cells due to its capacity of hemagglutination 97,98 ; they also affect blood cholesterol levels [99][100][101][102][103][104] and therefore participate in thrombosis. Already in 2009, Paraskevas et al 105 in a literature review considered the possible mechanisms involved between AAA and periodontitis, namely, the role of the inflammatory response and the effect on periodontal pathogens in the tissues of the host.…”

Section: Discussionmentioning

confidence: 99%

Can Periodontitis Influence the Progression of Abdominal Aortic Aneurysm? A Systematic Review

et al. 2018

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There is some evidence that periodontitis increases the risk of atherothrombosis. Abdominal aortic aneurysm (AAA) is a cardiovascular disease with specific risk factors and physiopathological mechanisms that can lead to rupture in the absence of treatment. The aim of the present systematic review was to explore the influence of periodontitis on the progression of AAAs as a specific disease. A systematic search in PubMed/MEDLINE and Embase databases was performed. Human and animal studies exploring the influence of periodontal pathogens on the progression of AAA were considered for inclusion. After systematic screening, 5 articles were included in the review. Due to the heterogeneity of the selected studies, a metaanalysis could not be performed. The descriptive analyses of the studies emphasized that periodontal pathogens or their by-products contribute to systemic and local innate immunity likely to be associated with AAA physiopathology. Periodontitis seems to play a role in the development and progression of AAA. The present systematic review suggests that the presence of periodontal bacteria in the bloodstream or in situ in the vascular lesion is a risk associated with aneurysmal disease progression.

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Effects of Porphyromonas gingivalis lipopolysaccharide on the expression of key genes involved in cholesterol metabolism in macrophages

Cited by 28 publications

References 27 publications

Two‐dimensional and three‐dimensional models for studying atherosclerosis pathogenesis induced by periodontopathogenic microorganisms

Two‐dimensional and three‐dimensional models for studying atherosclerosis pathogenesis induced by periodontopathogenic microorganisms

CD36 in chronic kidney disease: novel insights and therapeutic opportunities

Can Periodontitis Influence the Progression of Abdominal Aortic Aneurysm? A Systematic Review

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