New insights on atherosclerosis: A cross-talk between endocannabinoid systems with gut microbiota

Moludi, Jalal; Alizadeh, Mohammad; Yagin, Ned Lotfi; Pasdar, Yahiya; Nachvak, Seyed Mostafa; Abdollahzad, Hadi; Tabaei, Ali Sadeghpour

doi:10.15171/jcvtr.2018.21

Cited by 28 publications

(25 citation statements)

References 97 publications

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“…The bacterial metabolite trimethylamine is produced by the gut microbiota from dietary choline, phosphatidylcholine and l ‐carnitine, then oxidized to TMAO in the liver and released into the circulation . It has been suggested that TMAO contributes to atherosclerosis in part by promoting macrophage foam cell formation in atherosclerotic lesions as well as ineffective RCT and disruption of lipid homeostasis . For example, TMAO increased the macrophage expression of SR CD36, thereby promoting the uptake of modified LDL, and reduced the expression of enzymes involved in the synthesis of bile acids that are involved in RCT .…”

Section: Probiotics and Tmaomentioning

confidence: 99%

“…[75,76] However, interactions between probiotic bacteria, the gut, and the host immune systems are highly complex and despite increasingly growing clinical evidence, remain poorly understood. [75,76] In a recent study, a reduction in atherosclerotic lesion development was accompanied by the suppression of interferon--producing CD4 + T cells and pro-inflammatory cytokine production in Pediococcus acidilactici R037-treated mice. [45] In addition to a reduction in pro-inflammatory T cells, probiotic bacteria have been shown to decrease inflammation via an increase in regulatory T cells.…”

Section: Probiotics and Inflammationmentioning

confidence: 99%

“…[87] It has been suggested that TMAO contributes to atherosclerosis in part by promoting macrophage foam cell formation in atherosclerotic lesions as well as ineffective RCT and disruption of lipid homeostasis. [76,87,88] For example, TMAO increased the macrophage expression of SR CD36, thereby promoting the uptake of modified LDL, and reduced the expression of enzymes involved in the synthesis of bile acids that are involved in RCT. [35] In addition, TMAO has been shown to promote vascular inflammation, activation of arterial endothelial cells, and thrombosis.…”

Section: Probiotics and Tmaomentioning

confidence: 99%

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The Potential of Probiotics in the Prevention and Treatment of Atherosclerosis

O'Morain

Ramji

2019

Molecular Nutrition Food Res

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Atherosclerosis, the underlying cause of cardiovascular diseases such as myocardial infarction, cerebrovascular accident, and peripheral vascular disease, is the leading cause of global mortality. Current therapies against atherosclerosis, which mostly target the dyslipidemia associated with the disease, have considerable residual risk for cardiovascular disease together with various side effects. In addition, the outcomes from clinical trials on many promising pharmaceutical agents against atherosclerosis (e.g., low‐dose methotrexate, inhibitors against cholesteryl ester transfer protein) have been disappointing. Nutraceuticals such as probiotic bacteria have, therefore, generated substantial recent interest for the prevention of atherosclerosis and potentially as add‐ons with current pharmaceutical drugs. This review will discuss the current understanding of the anti‐atherogenic actions of probiotics from preclinical and clinical studies together with their potential underlying mechanisms of action.

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Section: Probiotics and Tmaomentioning

confidence: 99%

Section: Probiotics and Inflammationmentioning

confidence: 99%

Section: Probiotics and Tmaomentioning

confidence: 99%

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The Potential of Probiotics in the Prevention and Treatment of Atherosclerosis

O'Morain

Ramji

2019

Molecular Nutrition Food Res

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“…Numerous data have supported the contribution of dysbiosis in development of CVD by some mechanisms including increased gut permeability and metabolic endotoxemia [5][6][7]. This can be explained by a microbiome-derived lipopolysaccharide (LPS), a major component of the external membrane in gram-negative bacteria.…”

Section: Introductionmentioning

confidence: 99%

Effect of Probiotic Supplementation along with Calorie Restriction on Metabolic Endotoxemia, Trimethylamine-N-Oxide, Inflammation, Metabolic Factors, and Gut Microbiota Profile in Coronary Artery Disease Patients: A Double Blind Placebo Controlled Randomized Clinical Trial

Moludi

Kafil

Gholizadeh

et al. 2020

Preprint

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Background Dysbiosis has been associated to increased microbial translocation, leading to chronic inflammation in cardiovascular diseases (CVD). It has been proposed that modulation of gut microbiota by probiotic might modify metabolic endotoxemia. Therefore, the purpose of this study was to examine the effects of Lactobacillus rhamnosus GG (LGG) on metabolic endotoxemia, Trimethylamine-N-oxide (TMAO) and gut microbiota profiles in CVD subjects.Methods A 12-week randomized, double-blind, intervention on 44 patients with CVD. Patients were randomly allocated to receive either one LGG capsules 1.6 ×10 9 colony-forming unit (CFU) or the placebo capsules for 12 weeks. Gut microbiota profile and serum levels of interleukin‐1β (IL‐1β), Toll‐like receptor 4(TLR4), interleukin‐10(IL‐10), lipopolysaccharide(LPS), and TMAO were assessed before and after the intervention.Results A significant decrease in IL1-Beta concentration(-1.88 ± 2.25, vs. 0.56 ± 1.58 mmol/L, P=0.027), LPS levels(-5.20 ±2.70 vs. 2.96+ 5.27 mg/L, P=0.016), and TMAO levels (-19.34±20.40 vs. -6.45±7.7 mmol/L, P=0.043) was observed after the probiotic supplementation compared with the placebo. L. rhamnosus statically increased in intervention group while Bacteroidetes non - significantly increased in both groups. Subjects who had ≥2.5 kg weight loss showed signiﬁcantly improved in some variables, compared to patients with <2.5 kg weight reduction, regardless of the supplement they receive. Regression analysis revealed that baseline TMAO, changes of protein intakes and IL1-Beta predicted 58% of the final TMAO levels.Conclusion : These data provide preliminary evidence that probiotic supplementation has beneficial effects on depressive symptoms, metabolic endotoxemia, TMAO, and gut microbiota profile in subjects with CVD.

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“…In addition, patients with metabolic diseases are shown to be more likely to develop concurrent bacteraemia during dengue which also increased the likelihood of fatal dengue [22]. Therefore, it would be important to determine if low-grade endotoxaemia seen in patients with metabolic diseases [23], contribute to severe dengue and subsequently concurrent bacteraemia.…”

Section: Introductionmentioning

confidence: 99%

The association of lipopolysaccharide and inflammatory markers with severe dengue infection

Shyamali¹,

Mahaputuna²,

Gomes³

et al. 2019

Preprint

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Background Although serum lipopolysaccharide (LPS) was shown to associate with development of severe dengue, the reasons for high LPS and its subsequent involvement in disease pathogenesis are not known. Methods: We assessed LPS, lipopolysaccharide binding protein (LBP), CRP, IL-18, procalcitonin in patients with acute dengue fever (DF=129) and dengue haemorrhagic fever (DHF=64) and correlated these observations with the presence of comorbid illnesses, concurrent bacteraemia and clinical disease severity. Results: LPS levels were significantly (p=0.01) higher in patients with DHF, compared to those with DF. 45 (70%) of those with DHF and 63 (49%) of those with DF had detectable LPS and therefore, presence of LPS was significantly associated with DHF (p=0.005, OR=2.48, 95% CI: 1.29 to 4.64). Those with metabolic diseases, 22/29 (75.9%) and those with atopic diseases 17/22 (77.3%) were significantly more likely to have detectable LPS (p=0.025, OR=2.9, 95% CI- 1.17 to 7.59) and (p=0.039, OR=3.06, 95% CI-1.07 to 7.81) respectively, than others. LPS, LBP and CRP levels were high at the febrile phase, before onset of plasma leakage and reduced towards to the critical phase. The CRP levels were significantly higher (p=0.03) in early illness (≤3 days of illness) in those who progressed to develop DHF when compared to those who developed DF. Those who had detectable serum LPS also had a significantly higher CRP (p=0.01). Although there was no difference in procalcitonin (PCT) levels in patients with DF and DHF, the PCT levels were significantly higher in those who had detectable serum LPS (p=0.02). Conclusions: LPS levels were higher in patients with DHF and associated with high levels of other inflammatory markers. Since LPS levels were highest during early infection and were significantly more likely to be present in those with comorbid illnesses, the possible role of LPS in disease pathogenesis, should be further investigated.

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New insights on atherosclerosis: A cross-talk between endocannabinoid systems with gut microbiota

Cited by 28 publications

References 97 publications

The Potential of Probiotics in the Prevention and Treatment of Atherosclerosis

The Potential of Probiotics in the Prevention and Treatment of Atherosclerosis

Effect of Probiotic Supplementation along with Calorie Restriction on Metabolic Endotoxemia, Trimethylamine-N-Oxide, Inflammation, Metabolic Factors, and Gut Microbiota Profile in Coronary Artery Disease Patients: A Double Blind Placebo Controlled Randomized Clinical Trial

The association of lipopolysaccharide and inflammatory markers with severe dengue infection

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