Soluble TNF-α and interleukin-6 receptors in the urine of heart failure patients. Their clinical value and relationship with plasma levels

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

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Inflammation-Related Biomarkers Are Associated with Heart Failure Severity and Poor Clinical Outcomes in Patients with Non-Ischemic Dilated Cardiomyopathy

Life ◽

10.3390/life11101006 ◽

2021 ◽

Vol 11 (10) ◽

pp. 1006

Author(s):

Ieva Kažukauskienė ◽

Vaida Baltrūnienė ◽

Ieva Rinkūnaitė ◽

Edvardas Žurauskas ◽

Dalius Vitkus ◽

...

Keyword(s):

Heart Failure ◽

Dilated Cardiomyopathy ◽

Clinical Outcomes ◽

Interleukin 6 ◽

Cardiac Event ◽

Tnf Α ◽

Failure Severity ◽

Non Ischemic Dilated Cardiomyopathy ◽

Hs Crp ◽

Heart Failure Severity

Inflammation-related biomarkers are associated with clinical outcomes in mixed-etiology chronic heart failure populations. Inflammation-related markers tend to be higher in ischemic than in non-ischemic dilated cardiomyopathy (NI-DCM) patients, which might impact their prognostic performance in NI-DCM patients. Therefore, we aimed to assess the association of inflammation-related biomarkers with heart failure severity parameters and adverse cardiac events in a pure NI-DCM patient cohort. Fifty-seven patients with NI-DCM underwent endomyocardial biopsy. Biopsies were evaluated by immunohistochemistry for CD3+, CD45ro+, CD68+, CD4+, CD54+, and HLA-DR+ cells. Blood samples were tested for high-sensitivity C-reactive protein (hs-CRP), interleukin-6, tumor necrosis factor-α (TNF-α), soluble urokinase-type plasminogen activator receptor and adiponectin. During a five-year follow-up, twenty-seven patients experienced at least one composite adverse cardiac event: left ventricle assist device implantation, heart transplantation or death. Interleukin-6, TNF-α and adiponectin correlated with heart failure severity parameters. Patients with higher levels of interleukin-6, TNF-α, adiponectin or hs-CRP, or a higher number of CD3+ or CD45ro+ cells, had lower survival rates. Interleukin-6, adiponectin, and CD45ro+ cells were independently associated with poor clinical outcomes. All patients who had interleukin-6, TNF-α and adiponectin concentrations above the threshold experienced an adverse cardiac event. Therefore, a combination of these cytokines can identify high-risk NI-DCM patients.

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Plasma levels of pro-inflammatory molecules and their expressions are associated with severity of heart failure: An investigation in Chinese cohort

European Journal of Inflammation ◽

10.1177/2058739219836577 ◽

2019 ◽

Vol 17 ◽

pp. 205873921983657

Author(s):

Yongxi Xu ◽

Hongyan Sun ◽

Zhihao Wang ◽

Yufeng Wang

Keyword(s):

Heart Failure ◽

Plasma Levels ◽

Adult Population ◽

Interleukin 1 ◽

Heart Association ◽

Enzyme Linked Immunosorbent Assay ◽

Tnf Receptor ◽

Tnf Α ◽

Significant Difference ◽

Inflammatory Molecules

Heart failure (HF) is a syndrome with multiple clinical phenotypes affecting around 1%–2% of adult population worldwide, and about 230 million Chinese are affected by cardiovascular diseases. The important role of pro-inflammatory plasma cytokines with HF has been demonstrated in different populations. The aim of this study was to investigate importance of pro-inflammatory cytokines in Chinese HF patients. In all, 134 HF patients were enrolled in this study and further classified in to four clinical distinct groups according to New York Heart Association classification criteria (NYHA-I: n = 34, NYHA-II: n = 35, NYHA-III: n = 22 and NYHA-IV: n = 43). Sixty-eight healthy Chinese were enrolled as controls. Plasma levels of tumour necrosis factor-α (TNF-α), TNF-receptor 1 (TNFRI), TNF-receptor 2 (TNFRII), interleukin 6 (IL-6), soluble IL-6 receptor (sIL-6R), C-reactive protein (CRP), soluble cluster of differentiation 14 (sCD14) and interleukin 1 beta (IL-1β) were quantified by enzyme-linked immunosorbent assay (ELISA). Plasma levels of all parameters investigated in this study remained comparable among healthy controls and NYHA-I group. Plasma levels of TNF-α, TNFRI, TNFRII, IL-6, sIL-6R, CRP, sCD14 and IL-1β were significantly higher in NYHA-III and NYHA-IV clinical categories compared to other HF phenotype (NYHA-I and NYHA-II). Interestingly, TNFR-II levels were significantly higher in NYHA-II compared to NYHA-I. No significant difference of plasma sIL-6R was observed among various clinical categories. In conclusion, plasma levels of pro-inflammatory molecules are elevated in severe HF patients and may be used as possible biomarkers for accessing severity of HF.

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Nonlinear Indices of Heart Rate Variability in Chronic Heart Failure Patients: Redundancy and Comparative Clinical Value

Journal of Cardiovascular Electrophysiology ◽

10.1111/j.1540-8167.2007.00728.x ◽

2007 ◽

Vol 18 (4) ◽

pp. 425-433 ◽

Cited By ~ 83

Author(s):

ROBERTO MAESTRI ◽

GIAN DOMENICO PINNA ◽

AGOSTINO ACCARDO ◽

PAOLO ALLEGRINI ◽

RITA BALOCCHI ◽

...

Keyword(s):

Heart Failure ◽

Heart Rate ◽

Heart Rate Variability ◽

Chronic Heart Failure ◽

Clinical Value ◽

Heart Failure Patients

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Positive Pressure Ventilation Treatment Reduces Plasma Levels of Amino Terminal-Pro Brain Natriuretic Peptide in Congestive Heart Failure Patients With Sleep Apnea

Circulation Journal ◽

10.1253/circj.70.572 ◽

2006 ◽

Vol 70 (5) ◽

pp. 572-574 ◽

Cited By ~ 10

Author(s):

Zhi-Hui Zhao ◽

Zhi-Hong Liu ◽

Qin Luo ◽

Chang-Ming Xiong ◽

Xin-Hai Ni ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sleep Apnea ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Levels ◽

Positive Pressure Ventilation ◽

Positive Pressure ◽

Heart Failure Patients ◽

Amino Terminal

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Quantification of proinflammatory cytokines in the urine of congestive heart failure patients. Its relationship with plasma levels

European Journal of Heart Failure ◽

10.1016/s1388-9842(02)00165-4 ◽

2003 ◽

Vol 5 (1) ◽

pp. 27-31 ◽

Cited By ~ 18

Author(s):

Rafael Sirera ◽

Antonio Salvador ◽

Ildefonso Roldán ◽

Raquel Talens ◽

Andrés González-Molina ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Proinflammatory Cytokines ◽

Plasma Levels ◽

Heart Failure Patients

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Inflammation and its association with oxidative stress in dogs with heart failure

BMC Veterinary Research ◽

10.1186/s12917-021-02878-x ◽

2021 ◽

Vol 17 (1) ◽

Author(s):

Alenka Nemec Svete ◽

Barbara Verk ◽

Nina Čebulj-Kadunc ◽

Janez Salobir ◽

Vida Rezar ◽

...

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Blood Cell ◽

White Blood Cell ◽

Interleukin 6 ◽

Oxidative Stress Markers ◽

Stress Markers ◽

Markers Of Inflammation ◽

Tnf Α ◽

And Oxidative Stress

Abstract Background Inflammation and oxidative stress can contribute to the development and progression of heart failure. This study aimed to investigate the association between inflammatory and oxidative stress markers in dogs with congestive heart failure (CHF). Associations between the disease severity marker N-terminal pro-B-type natriuretic peptide (NT-proBNP) and markers of inflammation and oxidative stress were also determined. Results Thirty-seven dogs with cardiovascular diseases (dilated cardiomyopathy, DCM (16 dogs), myxomatous mitral valve disease, MMVD (21 dogs)) and ten healthy dogs were included in this prospective study. The patients were further divided into groups with (26) and without CHF (11). We found a significantly higher serum concentration of C-reactive protein (P = 0.012), white blood cell (P = 0.001), neutrophil (P = 0.001) and monocyte counts (P = 0.001) in patients with CHF compared to control dogs. The concentration of tumor necrosis factor-alpha (TNF-α) was significantly higher in patients with CHF compared to patients without CHF (P = 0.030). No significant difference was found in most of the measured parameters between MMVD and DCM patients, except for glutathione peroxidase (GPX) and NT-proBNP. In patients with CHF, TNF-α correlated positively with malondialdehyde (P = 0.014, r = 0.474) and negatively with GPX (P = 0.026, r = − 0.453), and interleukin-6 correlated negatively with GPX (P = 0.046, r = − 0.412). NT-proBNP correlated positively with malondialdehyde (P = 0.011, r = 0.493). In patients without CHF none of the inflammatory and oxidative stress markers correlated significantly. Furthermore, in the group of all cardiac patients, GPX activity significantly negatively correlated with NT-proBNP (P = 0.050, r = − 0.339) and several markers of inflammation, including TNF-α (P = 0.010, r = − 0.436), interleukin-6 (P = 0.026, r = − 0.382), white blood cell (P = 0.032, r = − 0.369), neutrophil (P = 0.027, r = − 0.379) and monocyte counts (P = 0.024, r = − 0.386). Conclusion Inflammatory and oxidative stress markers are linked in canine CHF patients, but not in patients without CHF. These results suggest complex cross communication between the two biological pathways in advanced stages of CHF.

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