interleukin-8 and Cardiomyopathies

BACKGROUND This retrospective, observational study from a single center aimed to evaluate the association between complement (C)3 and C4, lymphocytes markers CD4 and CD8, and the interleukins IL-1ß, IL-2R, IL-6, IL-10, and IL-8 in patients with sepsis-induced myocardial dysfunction (SIMD) and a reduced left ventricular ejection fraction (LVEF) of < 50%. MATERIAL AND METHODS Patients with sepsis from July 2017 to December 2020 were divided into a SIMD group (42 patients) and NO-SIMD group (214 patients). Diagnostic criteria of sepsis were based on SEPSIS 3.0 guidelines. SIMD was defined as LVEF.

Topics: Aged; Cardiomyopathies; Female; Humans; Interleukin-8; Male; Middle Aged; Retrospective Studies; Sepsis

The article presents the results of study of association of risk of development and clinical course of cardiomyopathies with polymorphic variants of genes ACE, GSTM1, IL8 and IL10. The purpose of research was to find out molecular genetic markers of risk of development and clinical course of various types of cardiomyopathies. The analysis used the DNA samples extracted from lymphocytes of peripheral venous blood of patients with cardiomyopathies (N = 89) and control group (N = 426). The standard analysis techniques of polymerase chain reaction and restriction fragment length polymorphism were applied to detect polymorphic loci of genes candidates. It is established that genotype of DD-polymorphic locus of I/DgeneACE is a marker of development of ischemic cardiomyopathy. The allele D is a marker of development of increased rate of manifestation of extra-systoles, growth of inter-ventricular septum and reduction of fraction of discharge in patients with cardiomyopathies.

Topics: Bashkiria; Cardiomyopathies; Female; Genetic Loci; Genotype; Glutathione Transferase; Humans; Interleukin-10; Interleukin-8; Male; Peptidyl-Dipeptidase A; Polymorphism, Genetic

Patients with chronic obstructive pulmonary disease (COPD) have elevated cardiovascular risk, and myocardial injury is common during severe exacerbations. Little is known about the prevalence, magnitude, and underlying mechanisms of cardiovascular risk in community-treated exacerbations.. To investigate how COPD exacerbations and exacerbation frequency impact cardiovascular risk and myocardial injury, and whether this is related to airway infection and inflammation.. We prospectively measured arterial stiffness (aortic pulse wave velocity [aPWV]) and cardiac biomarkers in 98 patients with stable COPD. Fifty-five patients had paired stable and exacerbation assessments, repeated at Days 3, 7, 14, and 35 during recovery. Airway infection was identified using polymerase chain reaction.. COPD exacerbation frequency was related to stable-state arterial stiffness (rho = 0.209; P = 0.040). Frequent exacerbators had greater aPWV than infrequent exacerbators (mean ± SD aPWV, 11.4 ± 2.1 vs. 10.3 ± 2.0 ms(-1); P = 0.025). Arterial stiffness rose by an average of 1.2 ms(-1) (11.1%) from stable state to exacerbation (n = 55) and fell slowly during recovery. In those with airway infection at exacerbation (n = 24) this rise was greater (1.4 ± 1.6 vs. 0.7 ± 1.3 ms(-1); P = 0.048); prolonged; and related to sputum IL-6 (rho = 0.753; P < 0.001). Increases in cardiac biomarkers at exacerbation were higher in those with ischemic heart disease (n = 12) than those without (n = 43) (mean ± SD increase in troponin T, 0.011 ± 0.009 vs. 0.003 ± 0.006 μg/L, P = 0.003; N-terminal pro-brain natriuretic peptide, 38.1 ± 37.7 vs. 5.9 ± 12.3 pg/ml, P < 0.001).. Frequent COPD exacerbators have greater arterial stiffness than infrequent exacerbators. Arterial stiffness rises acutely during COPD exacerbations, particularly with airway infection. Increases in arterial stiffness are related to inflammation, and are slow to recover. Myocardial injury is common and clinically significant during COPD exacerbations, particularly in those with underlying ischemic heart disease.

Topics: Aged; Aged, 80 and over; Aorta; Blood Pressure; C-Reactive Protein; Cardiomyopathies; Cardiovascular Diseases; Cohort Studies; Disease Progression; Female; Fibrinogen; Heart Rate; Humans; Interleukin-6; Interleukin-8; Male; Middle Aged; Myocardial Ischemia; Natriuretic Peptide, Brain; Peptide Fragments; Prospective Studies; Pulmonary Disease, Chronic Obstructive; Pulse Wave Analysis; Risk Factors; Spirometry; Sputum; Troponin T; Vascular Stiffness

Immunoreactive signal for the desmosomal protein plakoglobin (γ-catenin) is reduced at cardiac intercalated disks in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), a highly arrhythmogenic condition caused by mutations in genes encoding desmosomal proteins. Previously, we observed a false-positive case in which plakoglobin signal was reduced in a patient initially believed to have ARVC but who actually had cardiac sarcoidosis. Sarcoidosis can masquerade clinically as ARVC but has not been previously associated with altered desmosomal proteins.. We observed marked reduction in immunoreactive signal for plakoglobin at cardiac myocyte junctions in patients with sarcoidosis and giant cell myocarditis, both highly arrhythmogenic forms of myocarditis associated with granulomatous inflammation. In contrast, plakoglobin signal was not depressed in lymphocytic (nongranulomatous) myocarditis. To determine whether cytokines might promote dislocation of plakoglobin from desmosomes, we incubated cultures of neonatal rat ventricular myocytes with selected inflammatory mediators. Brief exposure to low concentrations of interleukin (IL)-17, tumor necrosis factor-α (TNF-α), and IL-6 (cytokines implicated in granulomatous myocarditis) caused translocation of plakoglobin from cell-cell junctions to intracellular sites, whereas other potent cytokines implicated in nongranulomatous myocarditis had no effect, even at much higher concentrations. We also observed myocardial expression of IL-17 and TNF-α and elevated levels of serum inflammatory mediators, including IL-6R, IL-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1β, in patients with ARVC (all P<0.0001 compared with controls).. The results suggest novel disease mechanisms involving desmosomal proteins in granulomatous myocarditis and implicate cytokines, perhaps derived in part from the myocardium, in disruption of desmosomal proteins and arrhythmogenesis in ARVC.

Topics: Adolescent; Adult; Aged; Animals; Arrhythmias, Cardiac; Autopsy; Biopsy; Cardiomyopathies; Case-Control Studies; Cells, Cultured; Chemokine CCL2; Chemokine CCL4; Child; Desmosomes; Female; gamma Catenin; Humans; Intercellular Junctions; Interleukin-17; Interleukin-6; Interleukin-8; Male; Middle Aged; Models, Animal; Myocarditis; Myocytes, Cardiac; Rats; Rats, Wistar; Sarcoidosis; Signal Transduction; Tumor Necrosis Factor-alpha; Ventricular Dysfunction, Right; Young Adult

Chronic heart failure (CHF) is associated with a higher risk for diabetes mellitus. Retinol binding protein 4 (RBP 4) is an adipose tissue-derived protein with pro-diabetogenic effects. A complete understanding of the association of CHF and insulin resistance remains elusive. The purpose of this study was to examine the relationship between CHF and diabetes mellitus.. Plasma levels of RBP 4, insulin, and interleukins (IL) 2, 8, and 10, were assessed in patients with dilated cardiomyopathy (DCM, n = 53), dilated inflammatory cardiomyopathy (DCMi, n = 54), and controls (n = 20). In addition, a possible mechanism of RBP 4 regulation was examined in adipocytes in vitro. Plasma levels of RBP 4 and insulin were measured by a specific ELISA. Interleukin concentrations were obtained by multiplex ELISA. Cell culture with 3T3-L1 adipocytes was performed to measure RBP 4 mRNA expression after stimulation with IL-8. RBP 4 levels were significantly increased in patients with DCMi (52.95 +/- 20.42 microg/mL) compared with DCM (35.54 +/- 23.08 microg/mL) and the control group (27.3 +/- 18.51 microg/mL). RBP 4 was positively correlated with IL-8 (r=0.416, P < 0.05) in human plasma in patients with DCMi. Moreover, increased insulin resistance was observed in patients with DCMi compared with the control and DCM groups. In vitro, IL-8 induced a significant upregulation of RBP 4 mRNA expression in adipocytes.. Elevated RBP 4 plasma concentrations, induced by IL-8, might be one mechanism leading to a higher incidence of diabetes in patients with DCMi.

Topics: 3T3 Cells; Adipocytes; Adult; Animals; Cardiomyopathies; Cardiomyopathy, Dilated; Cells, Cultured; Diabetes Complications; Enzyme-Linked Immunosorbent Assay; Female; Heart Failure; Humans; Inflammation; Insulin; Interleukin-10; Interleukin-2; Interleukin-8; Male; Mice; Middle Aged; Retinol-Binding Proteins, Plasma

Diminished cardiac contractility associated with inflammatory infiltration may be mediated by the release of interleukins. To test this hypothesis, we assessed the presence of interleukin and interleukin-receptor mRNAs in non-failing human heart and in endomyocardial biopsies from patients with dilated cardiomyopathy or inflammatory myocarditis. Only those interleukins expressed by non-circulating cells (interleukin-1 beta, -4, and -8) were detected in samples of human heart while interleukins specific for activated leukocytes (interleukins-1 alpha and -2) were not detected in any samples. While interleukin-1-receptor mRNA was present in samples from non-failing hearts and those with idiopathic myopathy, it was absent from patients with inflammatory myocarditis, suggesting receptor mRNA down-regulation.

Topics: Base Sequence; Cardiomyopathies; Cardiomyopathy, Dilated; Interleukin-1; Interleukin-2; Interleukin-4; Interleukin-8; Interleukins; Molecular Sequence Data; Myocarditis; Myocardium; Polymerase Chain Reaction; Receptors, Immunologic; Receptors, Interleukin-1; RNA, Messenger