Effects of recombinant tumour necrosis factor (rTNF-α) in cancer. Observations on the acute phase protein reaction and immunoglobulin synthesis after high dose recombinant TNF-α administration in isolated limb perfusions in cancer patients

1993 ◽  
Vol 23 (12) ◽  
pp. 812-818 ◽  
Author(s):  
A. J. G. SWAAK ◽  
D. LIENARD ◽  
H. SCHRAFFORDT KOOPS ◽  
F. J. LEJEUNE ◽  
A. M. M. EGGERMONT
Keyword(s):  
Cancer Patients ◽  
Tumour Necrosis Factor ◽  
Acute Phase ◽  
Tumour Necrosis ◽  
Acute Phase Protein ◽  
High Dose ◽  
Tnf Α ◽  
Phase Protein ◽  
Protein Reaction ◽  
Necrosis Factor

Relationship of serum levels of interleukin-6, soluble interleukin-6 receptor and tumour necrosis factor receptors to the acute-phase protein response in advanced pancreatic cancer

1999 ◽  
Vol 96 (1) ◽  
pp. 83-87 ◽  
Author(s):  
Matthew D. BARBER ◽  
Kenneth C. H. FEARON ◽  
James A. ROSS
Keyword(s):  
Tumour Necrosis Factor ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Tumour Necrosis ◽  
Acute Phase Protein ◽  
Serum Levels ◽  
Phase Protein ◽  
Interleukin 6 Receptor ◽  
Protein Response ◽  
Necrosis Factor

The level of the acute-phase response is a major predictor of survival in patients with advanced pancreatic cancer. This study examines the association between the acute-phase protein response, as determined by serum C-reactive protein, and serum levels of interleukin-6, soluble interleukin-6 receptor and the soluble tumour necrosis factor receptors in patients with pancreatic cancer. Thirty-four blood samples were collected from 13 patients with advanced pancreatic cancer. Samples were also collected from six healthy subjects. Levels of C-reactive protein, interleukin-6, soluble interleukin-6 receptor and soluble tumour necrosis factor receptors 55 and 75 were measured by indirect ELISA. Serum levels of C-reactive protein, interleukin-6 and soluble tumour necrosis factor receptors 55 and 75 were significantly higher in cancer patients than in controls. Levels of serum soluble interleukin-6 receptor were not significantly different between the two groups. In cancer patients, a significant positive association was found between the level of the acute-phase protein response and serum levels of interleukin-6, soluble tumour necrosis factor receptor 55 and soluble tumour necrosis factor receptor 75. No association was found between levels of soluble interleukin-6 receptor and any other factor. There is no significant relationship between the level of soluble interleukin-6 receptor and the acute-phase protein response in vivo and the biological role of soluble interleukin-6 receptor in the chronic inflammatory component of cachexia remains unclear.

Chicken amyloid arthropathy: serum amyloid A, interleukin-1β, interleukin-6, tumour necrosis factor-α and nitric oxide profile in acute phase (12th hour)

2013 ◽  
Vol 16 (2) ◽  
pp. 241-247 ◽  
Author(s):  
A. Sevimli ◽  
T. Bübül ◽  
A. Bulübül ◽  
A. Yaǧcı
Keyword(s):  
Nitric Oxide ◽  
Vitamin A ◽  
Tumour Necrosis Factor ◽  
Acute Phase ◽  
Tumour Necrosis ◽  
Serum Amyloid A ◽  
Amyloid A ◽  
Tnf Α ◽  
Amyloid Arthropathy ◽  
Necrosis Factor

Abstract Acute phase response (APR) is part of the early defense system, which is triggered by different stimuli including, infection, trauma, stres, inflammation and neoplasia. The APR complex is a reaction which induces homeostasis and recovery. In this research, serum amyloid A (SAA), interlaukin (IL)-1β, IL-6, tumour necrosis factor alpha (TNF-α) and nitric oxide (NO) levels were measured 12 hours following injection. For this purpose, Thirty-two 5 weeks old laying chicken were allocated into four groups and intra-articular injections of Freund’s adjuvant were used to induce amylod arthropathy in Groups II, III and IV. Vitamin A in group II, and methylprednisolone in group IV were added to enhance and to reduce the severity of amyloidosis, respectively. At the end of the research, it was observed that TNF-α and NO increased significantly (P<0.05) in vitamin A and methylprednisolone groups whereas SAA decreased significantly (P<0.05) in all groups. It was also observed that IL-6 increased (P<0.05) in vitamin A group and decreased in all other gorups however, IL-1β decreased in vitamin A and methylprednisolone groups, while it was increased in the control group. The results of this study suggest that there is a positive correlation between serum TNF-α levels in acute and chronic phase in chickens with amyloid arthropathy.

Response of tumour necrosis factor-α to delayed in vitro monocyte stimulation in patients with septic shock is related to outcome

2002 ◽  
Vol 102 (3) ◽  
pp. 315-320 ◽  
Author(s):  
Olivier APPOLONI ◽  
Jean-Louis VINCENT ◽  
Jean DUCHATEAU
Keyword(s):  
Septic Shock ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
High Dose ◽  
Tumour Necrosis Factor Α ◽  
Cell Stimulation ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

We hypothesized that cytokine production following delayed in vitro cell stimulation (to reproduce physiological cellular status at baseline) may be related to outcome in patients with septic shock. A total of 20 patients were included in a prospective clinical study, conducted in a medico-surgical intensive care unit in a university hospital. Blood samples were obtained at the onset of septic shock; these were treated to retain the cells, but to wash out autologous plasma (containing potential inflammatory stimuli such as cytokines, bacterial products and drugs) and replace it with foetal calf serum. Each treated sample was divided into two sets of four aliquots, to be stimulated either immediately or after an overnight period of resting incubation at 37°C. The rest period was to allow recovery from potentially reversible endogenous or pharmacologically induced alterations in cellular response, in order to reproduce a near physiological state at baseline. In vitro cellular challenges used low-dose (0.2ng/ml) or high-dose (1ng/ml) CD14-dependent lipopolysaccharide and CD14-independent pokeweed mitogen to induce the production of tumour necrosis factor-α (TNF-α), and interleukins-1β and -10. Levels of TNF-α, interleukin-1β and interleukin-10 were significantly higher (P < 0.05) when cell stimulation was delayed for 16h, indicating a functional down-regulation of cells during septic shock. Moreover, TNF-α responses obtained with high-dose lipopolysaccharide were significantly greater in cells from patients who subsequently survived septic shock (n = 13; median value 1392pg/ml; range 592-2048pg/ml) than in cells from non-survivors (n = 7; median value 708 pg/ml; range 520-1344pg/ml). These observations support the existence of individual differences in the inflammatory response that could influence patient outcome following septic shock.

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

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