Epicardial adipose tissue microbial colonization and inflammasome activation in acute coronary syndrome

Pedicino, Daniela; Severino, Anna; Ucci, Sarassunta; Bugli, Francesca; Flego, Davide; Giglio, Ada Francesca; Trotta, Francesco; Ruggio, Aureliano; Lucci, Claudia; Iaconelli, Antonio; Sterbini, Francesco Paroni; Biasucci, Luigi M.; Sanguinetti, Maurizio; Glieca, Franco; Luciani, Nicola; Massetti, Massimo; Crea, Filippo; Liuzzo, Giovanna

doi:10.1016/j.ijcard.2017.02.040

Cited by 32 publications

(30 citation statements)

References 14 publications

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“…In contrast, bacterial DNA was reported in mesenteric adipose tissue of 12 subjects with obesity belonging mostly to Ralstonia a year later [212]. Bacterial DNA was moreover detected in epicardial adipose tissue of subjects with acute coronary syndrome and stable angina, whereas none could be found in subjects with isolated mitral insufficiency [213]. The authors associated coronary heart disease with an increased susceptibility of the epicardial adipose tissue to bacterial colonization and inflammasome activation.…”

Section: Bacterial Presence In Remote Tissuesmentioning

confidence: 94%

Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

Chakaroun¹,

Massier²,

Kovacs³

2020

Nutrients

180

133

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The emerging evidence on the interconnectedness between the gut microbiome and host metabolism has led to a paradigm shift in the study of metabolic diseases such as obesity and type 2 diabetes with implications on both underlying pathophysiology and potential treatment. Mounting preclinical and clinical evidence of gut microbiota shifts, increased intestinal permeability in metabolic disease, and the critical positioning of the intestinal barrier at the interface between environment and internal milieu have led to the rekindling of the “leaky gut” concept. Although increased circulation of surrogate markers and directly measurable intestinal permeability have been linked to increased systemic inflammation in metabolic disease, mechanistic models behind this phenomenon are underdeveloped. Given repeated observations of microorganisms in several tissues with congruent phylogenetic findings, we review current evidence on these unanticipated niches, focusing specifically on the interaction between gut permeability and intestinal as well as extra-intestinal bacteria and their joint contributions to systemic inflammation and metabolism. We further address limitations of current studies and suggest strategies drawing on standard techniques for permeability measurement, recent advancements in microbial culture independent techniques and computational methodologies to robustly develop these concepts, which may be of considerable value for the development of prevention and treatment strategies.

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Section: Bacterial Presence In Remote Tissuesmentioning

confidence: 94%

Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

Chakaroun¹,

Massier²,

Kovacs³

2020

Nutrients

180

133

View full text Add to dashboard Cite

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“…Although this retrospective cohort study could not exclude the risk of traditional confounding cardiovascular factors, it suggests that stratifying patients based on hsCRP levels is beneficial for the prediction of cardiovascular disease risk [ 60 ]. Currently, hybrid positron emission tomography imaging, coronary computed tomography angiography (CCTA), and biomarkers of gut microbiota have been used to stratify cardiovascular risks [ 15 , 61 ]. Hybrid positron emission tomography imaging is useful in underlying cardiovascular inflammatory states [ 62 ]; however, its extensive clinical application is limited because of the prolonged exposure of patients to radiation and its expensive cost.…”

Section: Better Attenuation Of Coronary Rir Lowers the Risks Of Acmentioning

confidence: 99%

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Wang

Liu

Shao

et al. 2020

Journal of Immunology Research

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Acute coronary syndrome (ACS) is a major cause of acute death worldwide. Both innate and adaptive immunity regulate atherosclerosis progression, plaque stability, and thrombus formation. Immune and inflammation dysfunction have been indicated in the pathogenesis of ACS. The imbalance in the proatherogenic and antiatherogenic immune networks promotes the transition of plaques from a stable to unstable state and results in the occurrence of acute coronary events. The residual inflammatory risk (RIR) has received increasing attention in recent years, and lowering RIR has been expected to improve the outcomes of ACS patients. The CANTOS, COLCOT, and LoDoCo trials verified the benefits of reducing cardiovascular events using anti-inflammation therapies; however, most of the other studies focusing on lowering RIR produced negative or contradicting results. Therefore, restoring the balance in autoimmune regulation is essential because proatherogenic and antiatherogenic immunomodulatory effects are equally important in the complex human immune network. In this review, we summarized the recent evidence of the roles of proatherogenic and antiatherogenic immune networks in the pathogenesis of ACS and discussed how immune and inflammation contribute to atherosclerosis progression, plaque instability, and adverse cardiovascular events. We also provide a “from bench to bedside” perspective of a novel and promising personalized strategy in RIR intervention and therapeutic approaches for the treatment of ACS.

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“…As such, EAT sampled from subjects with CAD showed higher NFkappaB, c-Jun N-terminal kinase (JNK) activity, TLR-2 and TLR-4 expression levels, all indicative of macrophage recruitment and activation [42]. Of interest, a recent study using next-generation sequencing technologies demonstrated the presence of bacterial DNA into EAT surrounding diseased coronary arteries, suggesting that EAT is susceptible to microbial colonization that might, thereby, contribute to elicit a proinflammatory response [43].…”

Section: The Clinical Relevance Of Eat In Coronary Artery Diseasementioning

confidence: 99%

Epicardial adipose tissue: at the heart of the obesity complications

Guglielmi

Sbraccia

2017

Acta Diabetol

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In recent years, the anatomic and functional contiguity of epicardial adipose tissue (EAT) to myocardium and coronary arteries has gained increasing interest for its potential pathogenetic role in obesity-related cardiac diseases. Besides its known and attributed biochemical cardioprotective properties, it is becoming evident that, in metabolic disease states, EAT-secreted bioactive molecules may play an important role in the pathogenesis of coronary artery disease and cardiac arrhythmias. EAT-derived inflammatory cytokines and reactive oxidative species may, indeed, play a part in the development of a local proatherogenic milieu by paracrine and vasocrine mechanisms of interaction. In addition, initial clinical and in vitro studies have pointed out that EAT could be a determinant of the substrate of atrial fibrillation by contributing to the structural and electrical remodeling of myocardium. This article reviews the current state of knowledge on the association of EAT with cardiac dysfunction and the potential factors mediating the cross talk between this fat depot and the underlying cardiac structures.

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Epicardial adipose tissue microbial colonization and inflammasome activation in acute coronary syndrome

Cited by 32 publications

References 14 publications

Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Epicardial adipose tissue: at the heart of the obesity complications

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