scholarly journals Systemic Inflammation in Metabolic Syndrome: Increased Platelet and Leukocyte Activation, and Key Role of CX3CL1/CX3CR1 and CCL2/CCR2 Axes in Arterial Platelet-Proinflammatory Monocyte Adhesion

2019 ◽  
Vol 8 (5) ◽  
pp. 708 ◽  
Author(s):  
Patrice Marques ◽  
Aida Collado ◽  
Sergio Martinez-Hervás ◽  
Elena Domingo ◽  
Esther Benito ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Systemic Inflammation ◽  
Immune Cell ◽  
Flow Chamber ◽  
Low Grade ◽  
Monocyte Adhesion ◽  
The Metabolic Syndrome ◽  
Factor Α ◽  
Arterial Endothelium

Background: Metabolic syndrome is associated with low-grade systemic inflammation, which is a key driver of premature atherosclerosis. We characterized immune cell behavior in metabolic syndrome, its consequences, and the potential involvement of the CX3CL1/CX3CR1 and CCL2/CCR2 chemokine axes. Methods: Whole blood from 18 patients with metabolic syndrome and 21 age-matched controls was analyzed by flow cytometry to determine the leukocyte immunophenotypes, activation, platelet-leukocyte aggregates, and CX3CR1 expression. ELISA determined the plasma marker levels. Platelet-leukocyte aggregates adhesion to tumor necrosis factor-α (TNFα)-stimulated arterial endothelium and the role of CX3CL1/CX3CR1 and CCL2/CCR2 axes was investigated with the parallel-plate flow chamber. Results: When compared with the controls, the metabolic syndrome patients presented greater percentages of eosinophils, CD3+ T lymphocytes, Mon2/Mon3 monocytes, platelet-eosinophil and -lymphocyte aggregates, activated platelets, neutrophils, eosinophils, monocytes, and CD8+ T cells, but lower percentages of Mon1 monocytes. Patients had increased circulating interleukin-8 (IL-8) and TNFα levels and decreased IL-4. CX3CR1 up-regulation in platelet-Mon1 monocyte aggregates in metabolic syndrome patients led to increased CX3CR1/CCR2-dependent platelet-Mon1 monocyte adhesion to dysfunctional arterial endothelium. Conclusion: We provide evidence of generalized immune activation in metabolic syndrome. Additionally, CX3CL1/CX3CR1 or CCL2/CCR2 axes are potential candidates for therapeutic intervention in cardiovascular disorders in metabolic syndrome patients, as their blockade impairs the augmented arterial platelet-Mon1 monocyte aggregate adhesiveness, which is a key event in atherogenesis.

scholarly journals Novel Immune Features of the Systemic Inflammation Associated with Primary Hypercholesterolemia: Changes in Cytokine/Chemokine Profile, Increased Platelet and Leukocyte Activation

2018 ◽  
Vol 8 (1) ◽  
pp. 18
Author(s):  
Aida Collado ◽  
Patrice Marques ◽  
Elena Domingo ◽  
Eva Perello ◽  
Herminia González-Navarro ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Immune Cell ◽  
Leukocyte Adhesion ◽  
Flow Chamber ◽  
Enzyme Linked Immunosorbent Assay ◽  
Low Grade ◽  
Leukocyte Activation ◽  
Primary Hypercholesterolemia ◽  
Th17 Lymphocytes ◽  
Arterial Endothelium

Primary hypercholesterolemia (PH) is associated with a low grade systemic inflammation that is likely the main driver of premature atherosclerosis. Accordingly, we characterized the immune cell behaviour in PH and its potential consequences. Whole blood from 22 PH patients and 21 age-matched controls was analysed by flow cytometry to determine the percentage of leukocyte immunophenotypes, activation, and platelet-leukocyte aggregates. Plasma markers were determined by Enzyme-Linked ImmunoSorbent Assay (ELISA). The adhesion of platelet-leukocyte aggregates to tumor necrosis factor-α (TNFα)-stimulated arterial endothelium was investigated using the dynamic model of the parallel-plate flow chamber. PH patients presented greater percentage of Mon 3 monocytes, Th2 and Th17 lymphocytes, activated platelets, and leukocytes than controls. The higher percentages of circulating platelet-neutrophil, monocyte and lymphocyte aggregates in patients caused increased platelet-leukocyte adhesion to dysfunctional arterial endothelium. Circulating CXCL8, CCL2, CX3CL1, and IL-6 levels positively correlated with key lipid features of PH, whereas negative correlations were found for IL-4 and IL-10. We provide the first evidence that increased platelet and leukocyte activation leads to elevated platelet-leukocyte aggregates in PH and augmented arterial leukocyte adhesiveness, a key event in atherogenesis. Accordingly, modulation of immune system behavior might be a powerful target in the control of further cardiovascular disease in PH.

scholarly journals Inflammation as a Link between Obesity and Metabolic Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Faloia Emanuela ◽  
Michetti Grazia ◽  
De Robertis Marco ◽  
Luconi Maria Paola ◽  
Furlani Giorgio ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Visceral Obesity ◽  
Low Grade ◽  
Subsequent Increase ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Inflammatory State

The metabolic syndrome is a complex of clinical features leading to an increased risk for cardiovascular disease and type 2 diabetes mellitus in both sexes. Visceral obesity and insulin resistance are considered the main features determining the negative cardiovascular profile in metabolic syndrome. The aim of this paper is to highlight the central role of obesity in the development of a chronic low-grade inflammatory state that leads to insulin resistance, endothelial and microvascular dysfunctions. It is thought that the starting signal of this inflammation is overfeeding and the pathway origins in all the metabolic cells; the subsequent increase in cytokine production recruits immune cells in the extracellular environment inducing an overall systemic inflammation. This paper focuses on the molecular and cellular inflammatory mechanisms studied until now.

Effect of a single high-fat meal on endothelial function in patients with the metabolic syndrome: Role of tumor necrosis factor-α

2007 ◽  
Vol 17 (4) ◽  
pp. 274-279 ◽  
Author(s):  
Katherine Esposito ◽  
Miryam Ciotola ◽  
Ferdinando C. Sasso ◽  
Domenico Cozzolino ◽  
Franco Saccomanno ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
High Fat ◽  
The Metabolic Syndrome ◽  
Factor Α ◽  
Necrosis Factor ◽  
Fat Meal

scholarly journals Obesity and asthma: co-morbidity or causal relationship?

2016 ◽  
Vol 73 (3) ◽  
Author(s):  
A. Van Huisstede ◽  
G.J. Braunstahl
Keyword(s):  
Metabolic Syndrome ◽  
Systemic Inflammation ◽  
Low Grade ◽  
Fat Tissue ◽  
Rigorous Approach ◽  
The Metabolic Syndrome ◽  
Bronchial Inflammation ◽  
Co Morbidity ◽  
Few Data ◽  
The Relationship

There is substantial evidence that obesity and asthma are related. “Obese asthma” may be a unique phenotype of asthma, characterized by decreased lung volumes, greater symptoms for a given degree of lung function impairment, destabilization or lack of asthma control, lack of eosinophilic inflammation and a different response to controller medication. Whether this relationship between obesity and asthma is causal or represents co-morbidity due to other factors is unclear. In previous reviews concerning the relationship between obesity and asthma, five hypotheses were put forth. One of these hypotheses is that a low grade systemic inflammation caused by adipokines from the fat tissue causes or enhances bronchial inflammation. In animal models, there is an increasing amount of evidence for the role of adipokines derived from fat tissue in the relationship between obesity and asthma. The data are conflicting in humans. Since obesity is a component of the metabolic syndrome and the metabolic syndrome is also a form of systemic inflammation, it is to be expected that there is a relationship between metabolic syndrome and asthma. The few data that are available show that there is no relationship between metabolic syndrome and asthma, but there is one between the metabolic syndrome and asthma-like symptoms. Further research is needed to confirm the relationship between obesity and asthma in humans, where a rigorous approach in the diagnosis of asthma is essential.

Role of genetic factors in the development of hypertension in young patients with metabolic syndrome

2020 ◽  
pp. 23-32
Author(s):  
Elena Korneeva ◽  
Mikhail Voevoda ◽  
Sergey Semaev ◽  
Vladimir Maksimov
Keyword(s):  
Metabolic Syndrome ◽  
High Risk ◽  
Arterial Hypertension ◽  
Genetic Factors ◽  
Young Patients ◽  
Integrin Αiibβ3 ◽  
Ace Gene ◽  
The Metabolic Syndrome

Results of the study related to polymorphism of ACE gene (rs1799752)‎, integrin αIIbβ3, and CSK gene (rs1378942) influencing development of arterial hypertension in young patients with metabolic syndrome are presented. Hypertension as a component of the metabolic syndrome was detected in 15.0% of young patients. Prevalence of mutant alleles of the studied genes among the examined patients was quite high, so homozygous DD genotype was found in 21.6%, and mutant D allele of the ACE gene in 47.4%. A high risk of hypertension in patients with MS was detected in carriers of the T allele of the CSK (rs1378942) gene – 54.8%, which was most often observed in a combination of polymorphic ACE and CSK gene loci (p = 0.0053).

scholarly journals Problems of Pathogenesis and Pathogenetic Therapy of COVID-19 from the Perspective of the General Theory of Pathological Systems (General Pathological Processes)

2021 ◽  
Vol 22 (14) ◽  
pp. 7582
Author(s):  
Evgenii Gusev ◽  
Alexey Sarapultsev ◽  
Desheng Hu ◽  
Valeriy Chereshnev
Keyword(s):  
Systemic Inflammation ◽  
Pathological Process ◽  
The State ◽  
The Other ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
The Metabolic Syndrome ◽  
Other Hand ◽  
Pathogenetic Therapy ◽  
Fundamental Medicine

The COVID-19 pandemic examines not only the state of actual health care but also the state of fundamental medicine in various countries. Pro-inflammatory processes extend far beyond the classical concepts of inflammation. They manifest themselves in a variety of ways, beginning with extreme physiology, then allostasis at low-grade inflammation, and finally the shockogenic phenomenon of “inflammatory systemic microcirculation”. The pathogenetic core of critical situations, including COVID-19, is this phenomenon. Microcirculatory abnormalities, on the other hand, lie at the heart of a specific type of general pathological process known as systemic inflammation (SI). Systemic inflammatory response, cytokine release, cytokine storm, and thrombo-inflammatory syndrome are all terms that refer to different aspects of SI. As a result, the metabolic syndrome model does not adequately reflect the pathophysiology of persistent low-grade systemic inflammation (ChSLGI). Diseases associated with ChSLGI, on the other hand, are risk factors for a severe COVID-19 course. The review examines the role of hypoxia, metabolic dysfunction, scavenger receptors, and pattern-recognition receptors, as well as the processes of the hemophagocytic syndrome, in the systemic alteration and development of SI in COVID-19.

Metabolic activity of visceral fat and immune-related organs evaluated by 18F-FDG PET/CT is associated with the metabolic syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Pahk ◽  
H.W Kwon ◽  
J.S Eo ◽  
H.S Seo ◽  
S Kim
Keyword(s):  
Metabolic Syndrome ◽  
Systemic Inflammation ◽  
Metabolic Activity ◽  
Fdg Pet ◽  
Inflammatory Activity ◽  
The Metabolic Syndrome ◽  
Inflammatory Status ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct

Abstract Background The risk of cardiovascular disease (CVD) is elevated in metabolic syndrome (MS) and is related to the inflammatory activity of visceral adipose tissue (VAT). We investigated whether the metabolic activity in VAT, assessed by 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT), is associated with systemic inflammatory status, and related to the number of MS components. Methods 18F-FDG PET/CT was performed in a total of 203 subjects: 59 without an MS component; M(0), 92 with one or two MS components; M(1–2), and 52 with MS. Metabolic activity of VAT was evaluated using the mean standardized uptake value (SUVmean) and the maximum SUV (SUVmax). Metabolic activities of immune-related organs such as spleen and bone marrow (BM) were evaluated using the SUVmax. Results VAT SUVmax correlated with high-sensitivity C-reactive protein (hsCRP) and the SUVmax of spleen and BM, which reflect the status of systemic inflammation. Both hsCRP and the SUVmax of the spleen and BM were higher in the MS group than in the M(1–2) or M(0) groups. In VAT, SUVmax increased with increasing number of MS components, while SUVmean decreased. Conclusions The SUVmax of VAT assessed by 18F-FDG PET/CT could reflect the inflammatory activity of VAT which is increased in the MS patients with systemic inflammation. Funding Acknowledgement Type of funding source: None

The Role of Quinapril in the Presence of a Weight Loss Regimen: Endothelial Function and Markers of Obesity in Patients With the Metabolic Syndrome

2007 ◽  
Vol 10 (4) ◽  
pp. 204-209 ◽  
Author(s):  
Sameer Nagamia ◽  
Anbu Pandian ◽  
Faiz Cheema ◽  
Rama Natarajan ◽  
Qamar A. Khan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Endothelial Function ◽  
The Metabolic Syndrome
Sign in / Sign up

Export Citation Format

Share Document