Effects of micro‐amounts of <i>Porphyromonas gingivalis</i> lipopolysaccharide on rabbit inflammatory immune response and development of atherosclerosis

Lin, Guo; Shi, Xiulin; Chen, S.; Lei, Lang; You, Xiaoqing; Huang, Min; Luo, Lan; Li, Y.; Zhao, Xin; Yan, Fuhua

doi:10.1111/jre.12214

Cited by 8 publications

(13 citation statements)

References 18 publications

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“…Similarly, a diet containing 1% cholesterol, 5% lard, and 15% yolk had no effect on ABL after 14 weeks in rabbits in absence of additional stimuli, but ABL induced by the exposition to P. gingivalis or A. actinomycetemcomitans during the last 6 weeks was exacerbated [51]. Similarly, higher ABL has been found in different studies in rodent periodontitis models when animals received different diets rich in saturated fats and/or cholesterol [52][53][54][55][56][57][58]. Interestingly, macrophage presence was evident in all groups receiving the experimental diet (HFD and HFD + LPS), a feature that did not depend on LPS administration.…”

Section: Discussionmentioning

confidence: 90%

A Diet Rich in Saturated Fat and Cholesterol Aggravates the Effect of Bacterial Lipopolysaccharide on Alveolar Bone Loss in a Rabbit Model of Periodontal Disease

et al. 2020

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Increasing evidence connects periodontitis with a variety of systemic diseases, including metabolic syndrome, atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). The proposal of this study was to evaluate the role of diets rich in saturated fat and cholesterol in some aspects of periodontal diseases in a lipopolysaccharide (LPS)-induced model of periodontal disease in rabbits and to assess the influence of a periodontal intervention on hyperlipidemia, atherosclerosis, and NAFLD progression to non-alcoholic steatohepatitis. Male rabbits were maintained on a commercial standard diet or a diet rich in saturated fat (3% lard w/w) and cholesterol (1.3% w/w) (HFD) for 40 days. Half of the rabbits on each diet were treated 2 days per week with intragingival injections of LPS from Porphyromonas gingivalis. Morphometric analyses revealed that LPS induced higher alveolar bone loss (ABL) around the first premolar in animals receiving standard diets, which was exacerbated by the HFD diet. A higher score of acinar inflammation in the liver and higher blood levels of triglycerides and phospholipids were found in HFD-fed rabbits receiving LPS. These results suggest that certain dietary habits can exacerbate some aspects of periodontitis and that bad periodontal health can contribute to dyslipidemia and promote NAFLD progression, but only under certain conditions.

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Section: Discussionmentioning

confidence: 90%

A Diet Rich in Saturated Fat and Cholesterol Aggravates the Effect of Bacterial Lipopolysaccharide on Alveolar Bone Loss in a Rabbit Model of Periodontal Disease

et al. 2020

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“…Meanwhile, endothelial cells are the targets of many endogenous and exogenous agents (e.g., LPS) that activate the endothelium and secret a variety of inflammatory mediators such as IL-1β, TNF-α, IL-6 and other neurotoxic substances [32]. There is considerable evidence that LPS contributes to the propagation of atherosclerosis, which has many features in common with inflammatory diseases [33]. In the present study, our results indicated that puerarin-V suppressed inflammatory cytokines release in vivo and in vitro experiments.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effects of Puerarin-V on Isoproterenol-Induced Myocardial Infarction Mice Is Associated with Regulation of PPAR-Υ/NF-κB Pathway

Yuan

Chen

et al. 2018

Molecules

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Puerarin is a well-known traditional Chinese medicine which has been used for the treatment of cardiovascular diseases. Recently, a new advantageous crystal form of puerarin, puerarin-V, has been developed. However, the cardioprotective effects of puerarin-V on myocardial infarction (MI) heart failure are still unclear. In this research, we aim to evaluate the cardioprotective effects of puerarin-V on the isoproterenol (ISO)-induced MI mice and elucidate the underlying mechanisms. To induce MI in C57BL/6 mice, ISO was administered at 40 mg/kg subcutaneously every 12 h for three times in total. The mice were randomly divided into nine groups: (1) control; (2) ISO; (3) ISO + puerarin injection; (4–9) ISO + puerarin-V at different doses and timings. After treatment, cardiac function was evaluated by electrocardiogram (ECG), biochemical and histochemical analysis. In vitro inflammatory responses and apoptosis were evaluated in human coronary artery endothelial cells (HCAECs) challenged by lipopolysaccharide (LPS). LPS-induced PPAR-Υ/NF-κB and subsequently activation of cytokines were assessed by the western blot and real-time polymerase chain reaction (PCR). Administration of puerarin-V significantly inhibits the typical ST segment depression compared with that in MI mice. Further, puerarin-V treatment significantly improves ventricular wall infarction, decreases the incidence of mortality, and inhibits the levels of myocardial injury markers. Moreover, puerarin-V treatment reduces the inflammatory milieu in the heart of MI mice, thereby blocking the upregulation of proinflammatory cytokines (TNF-α, IL-1β and IL-6). The beneficial effects of puerarin-V might be associated with the normalization in gene expression of PPAR-Υ and PPAR-Υ/NF-κB /ΙκB-α/ΙΚΚα/β phosphorylation. In the in vitro experiment, treatment with puerarin-V (0.3, 1 and 3 μM) significantly reduces cell death and suppresses the inflammation cytokines expression. Likewise, puerarin-V exhibits similar mechanisms. The cardioprotective effects of puerarin-V treatment on MI mice in the pre + post-ISO group seem to be more prominent compared to those in the post-ISO group. Puerarin-V exerts cardioprotective effects against ISO-induced MI in mice, which may be related to the activation of PPAR-γ and the inhibition of NF-κB signaling in vivo and in vitro. Taken together, our research provides a new therapeutic option for the treatment of MI in clinic.

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“…4 , Supplementary Figure 2 ) and a significant increase in the chemotactic effect on THP-1 monocytes by P. gingivalis [32] , [39] , [47] . The studies based on animal models exposed to P. gingivalis and E. corrodens reported a significant increase of NF-κβ [1] , [35] , [37] , [61] and those that were exposed to P. gingivalis, S. sanguinis and S. anginosus, reported a significant increase of TLR2 and TLR4 in peripheral blood and aortic tissue [35] , [50] , [61] ( Supplementary Figure 3 ).…”

Section: Discussionmentioning

confidence: 99%

Integrative analysis of gene and protein expression in atherosclerosis-related pathways modulated by periodontal pathogens. Systematic review

Marroquin

Guauque-Olarte

2023

Japanese Dental Science Review

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Effects of micro‐amounts of Porphyromonas gingivalis lipopolysaccharide on rabbit inflammatory immune response and development of atherosclerosis

Abstract: Micro-amounts of Pg-lipopolysaccharide induced the high expressions of inflammatory factors and mediated the inflammatory response. Pg-lipopolysaccharide elevated the blood lipid level less significantly than the high-fat diet did, but it may promote atherosclerosis.

Cited by 8 publications

References 18 publications

A Diet Rich in Saturated Fat and Cholesterol Aggravates the Effect of Bacterial Lipopolysaccharide on Alveolar Bone Loss in a Rabbit Model of Periodontal Disease

A Diet Rich in Saturated Fat and Cholesterol Aggravates the Effect of Bacterial Lipopolysaccharide on Alveolar Bone Loss in a Rabbit Model of Periodontal Disease

Cardioprotective Effects of Puerarin-V on Isoproterenol-Induced Myocardial Infarction Mice Is Associated with Regulation of PPAR-Υ/NF-κB Pathway

Integrative analysis of gene and protein expression in atherosclerosis-related pathways modulated by periodontal pathogens. Systematic review

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