Correlation of the serum concentrations of tumour necrosis factor and nitric oxide with disease severity in chronic Chagas disease (American trypanosomiasis)

2007 ◽  
Vol 101 (2) ◽  
pp. 123-132 ◽  
Author(s):  
R. Pérez-Fuentes ◽  
A. López-Colombo ◽  
G. Ordóñez-Toquero ◽  
I. Gomez-Albino ◽  
J. Ramos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumour Necrosis Factor ◽  
Disease Severity ◽  
Chagas Disease ◽  
Tumour Necrosis ◽  
Serum Concentrations ◽  
American Trypanosomiasis ◽  
Chronic Chagas Disease ◽  
Necrosis Factor

Interleukin-10 and tumour necrosis factor-alpha serum levels in chronic Chagas disease patients

2015 ◽  
Vol 37 (7) ◽  
pp. 376-379 ◽  
Author(s):  
R. H. T. Vasconcelos ◽  
E. de A. N. Azevedo ◽  
G. T. N. Diniz ◽  
M. da G. A. de M. Cavalcanti ◽  
W. de Oliveira ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Chagas Disease ◽  
Tumour Necrosis ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Chronic Chagas Disease ◽  
Necrosis Factor

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.

scholarly journals CD40 and tumour necrosis factor‐α co‐operate to up‐regulate inducuble nitric oxide synthase expression in macrophages

Immunology ◽  
2012 ◽  
Vol 135 (2) ◽  
pp. 140-150 ◽  
Author(s):  
Jose‐Andres C. Portillo ◽  
Luis Muniz Feliciano ◽  
Genevieve Okenka ◽  
Frederick Heinzel ◽  
M. Cecilia Subauste ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Hyperdynamic Circulation of Cirrhotic Rats with Ascites: Role of Endotoxin, Tumour Necrosis Factor-α and Nitric Oxide

1997 ◽  
Vol 93 (3) ◽  
pp. 219-225 ◽  
Author(s):  
Chi-Jen Chu ◽  
Fa-Yauh Lee ◽  
Sun-Sang Wang ◽  
LU Rei-Hwa ◽  
Yang-Te Tsai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumour Necrosis Factor ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Colorimetric Assay ◽  
Plasma Concentrations ◽  
No Production ◽  
Hyperdynamic Circulation ◽  
Tnf Α ◽  
Necrosis Factor

1. Hyperdynamic circulation observed in portal hypertensive states is characterized by generalized vasodilatation, increased cardiac index and increased systemic and regional blood flows. Endotoxin, tumour necrosis factor-alpha (TNF-α) and nitric oxide (NO) have been reported to be involved in the pathogenesis of hyperdynamic circulation, but the interactions between endotoxin, TNF-α and NO in cirrhotic rats with ascites have never been specifically addressed. 2. This study was designed to determine systemic and portal haemodynamics and plasma levels of endotoxin, TNF-α and nitrate/nitrite in cirrhotic rats with ascites and investigate the relationships between these substances. 3. Plasma concentrations of endotoxin, TNF-α and nitrate/nitrite (an index of NO production) were determined in 25 cirrhotic rats with ascites and 17 control rats using the Limulus assay, ELISA and a colorimetric assay respectively. In addition, haemodynamic studies were performed in another ten cirrhotic rats with ascites and ten control rats. 4. Cirrhotic rats with ascites had hyperdynamic circulation accompanied by increased plasma levels of endotoxin, TNF-α and nitrate/nitrite, as compared with control rats. Significant correlation existed between plasma levels of endotoxin and nitrate/nitrite (r = 0.59, P < 0.0001) and between plasma levels of endotoxin and TNF-α (r = 0.63, P < 0.0001). No correlation was detected between plasma levels of TNF-α and nitrate/nitrite (r = 0.24, P > 0.05). 5. This study suggests that endotoxaemia developed in cirrhotic rats with ascites may stimulate NO formation directly or indirectly via cytokine cascade, and consequently participate in the development and/or maintenance of hyperdynamic circulation.

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