scholarly journals Tumour necrosis factor α (TNF-α), interleukin-6 (IL-6) and their soluble receptors (sTNF-α-Rp55 and slL-6R) serum levels in systemic lupus erythematodes

1996 ◽  
Vol 5 (6) ◽  
pp. 435-441 ◽  
Author(s):  
E. Robak ◽  
A. Sysa-Jędrzejowska ◽  
T. Robak ◽  
H. Stępień ◽  
A. Woźniacka ◽  
...  
Keyword(s):  
Tumour Necrosis ◽  
Serum Levels ◽  
Serum Concentrations ◽  
Tumour Necrosis Factor Α ◽  
Systemic Lupus ◽  
Soluble Receptors ◽  
Normal Individuals ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

We investigated a possible association between serum concentrations of tumour necrosis factor α (TNF-α), interleukin-6 (IL-6) and their soluble receptors (sTNF-α-Rp55 and sIL-6R) using an enzyme-linked immunosorbent assay (ELISA) in 55 patients with systemic lupus erythematodes (SLE) and 16 healthy controls. We also examined a possible association between the serum levels of these peptides and SLE activity, as well as TNF-α and IL-6 concentrations and the levels of their soluble receptors. The median concentrations of TNF-α, sTNF-α-Rp55 and IL-6 were significantly higher in SLE patients than in normal individuals. In contrast, there was no difference between the serum level of sIL-6R in both groups. We found positive correlations between the serum concentrations of TNF-α and IL-6 as well as their soluble receptors and disease activity. There were also correlations between TNF-α and sTNF-α-Rp55 as well as IL-6 and sIL-6R serum levels in SLE patients but there were no such correlations in the normal control group. In conclusion, an increase in the serum levels of TNF-α, sTNF-α-Rp55 and IL-6 may become useful markers for SLE activity. Patients with SLE have sIL-6R serum concentration similar to that as in normal individuals. However, it correlates with disease activity and the level of IL-6.

Levels of Serum Interleukin (IL)-6, IL-1β, Tumour Necrosis Factor-α and Leptin and Their Correlation in Depression

2007 ◽  
Vol 41 (3) ◽  
pp. 266-273 ◽  
Author(s):  
Kun Yang ◽  
Guangrong Xie ◽  
Zhongxing Zhang ◽  
Changhong Wang ◽  
Wenbo Li ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Serum Levels ◽  
Tumour Necrosis Factor Α ◽  
Depressed Patients ◽  
Tnf Α ◽  
Male Patients ◽  
Factor Α ◽  
Normal Controls ◽  
Necrosis Factor

Objective: To investigate the relationship between leptin and cytokines in depressed patients. Methods: Thirty-three unmedicated patients (24 female, nine male) with depressive disorder and 23 healthy controls (16 female, seven male) were assessed for serum levels of interleukin (IL)-6, IL-1β, tumour necrosis factor-α (TNF-α) and leptin. Results: Levels of IL-6 and TNF-α in depressed patients were higher than in normal controls. There were significantly lower leptin levels in depressed patients than in normal controls. There were also significant differences in the leptin levels, being higher in female than in male patients, and in female than in male controls. Conclusions: IL-6 and TNF-α cytokines and leptin are important in the psychoimmunology of depressed patients. There were gender differences in leptin levels in depression.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

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

scholarly journals Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Abbas Jawad Al-Shabany ◽  
Alan John Moody ◽  
Andrew David Foey ◽  
Richard Andrew Billington
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Cytokine ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage ◽  
Necrosis Factor

Bacterial lipopolysaccharide induces changes in intracellular NAD+ levels in a pro-inflammatory, but not an anti-inflammatory, macrophage model that are correlated with the release of the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α).

Model for Whole Body Production of Tumour Necrosis Factor-α in Experimental Endotoxaemia in Healthy Subjects

1994 ◽  
Vol 87 (4) ◽  
pp. 459-465 ◽  
Author(s):  
R. Koopmans ◽  
F. J. Hoek ◽  
S. J. H. van Deventer ◽  
T. van der Poll
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Whole Body ◽  
Serum Concentrations ◽  
Tumour Necrosis Factor Α ◽  
Human Tumour ◽  
Human Tumour Necrosis Factor ◽  
Body Production ◽  
Factor Α ◽  
Necrosis Factor

1. Tumour necrosis factor-α is considered an important mediator in the pathophysiology of several diseases. Although much information is available about the serum concentrations of this cytokine in these illnesses, little is known about the production of tumour necrosis factor-α in disease in vivo. 2. In the present study we aimed to estimate the extent and the kinetics of whole body tumour necrosis factor-α synthesis in experimental endotoxaemia in six healthy humans. For this purpose we first examined the pharmacokinetic behaviour of an intravenously injected bolus of recombinant human tumour necrosis factor-α (50 μg/m2) in another group of six normal subjects. We then calculated the total amount of tumour necrosis factor-α produced after intravenous injection of endotoxin (2 ng/kg) as the product of the systemic clearance of recombinant human tumour necrosis factor-α (9.5 ± 5.0 ml min−1 kg−1) and the area under the tumour necrosis factor-α concentration-time curves in the endotoxaemic subjects. 3. Recombinant human tumour necrosis factor-α showed evident two-compartment kinetics with an initial rapid disappearance (t1/2 5.1 ± 2.2 min) and a terminal slower elimination (t1/2 49 ± 5 min). Tumour necrosis factor-α synthesis after endotoxin varied markedly between individuals, ranging from 11.8 to 114.1 μg (52.7 ± 34.7 μg). The changes in time of the serum concentrations of tumour necrosis factor-α after administration of endotoxin could be accurately described with an adapted two-compartment open model that incorporated both rapid tumour necrosis factor-α production (74% of the total amount) and slow tumour necrosis factor-α production (26%). 4. Our results suggest that, in endotoxaemia, circulating tumour necrosis factor-α originates from two different sources, one in rapid and one in slow equilibrium with the circulation. We propose that the pharmacokinetic characteristics of intravenous recombinant human tumour necrosis factor-α may be used to estimate the production of rumour necrosis factor-α in clinical disease.

Sign in / Sign up

Export Citation Format

Share Document