Polymorphisms in tumor necrosis factor and other cytokines as risks for infectious diseases and the septic syndrome

2001 ◽  
Vol 3 (5) ◽  
pp. 427-439 ◽  
Author(s):  
Julian Knight
Keyword(s):  
Tumor Necrosis Factor ◽  
Infectious Diseases ◽  
Tumor Necrosis ◽  
Septic Syndrome ◽  
Necrosis Factor

Effect of Chronic Administration of Recombinant Bovine Tumor Necrosis Factor to Cattle

1989 ◽  
Vol 26 (6) ◽  
pp. 462-472 ◽  
Author(s):  
H. Bielefeldt Ohmann ◽  
M. Campos ◽  
M. Snider ◽  
N. Rapin ◽  
T. Beskorwayne ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Infectious Diseases ◽  
Tumor Necrosis ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Prolonged Treatment ◽  
Chronic Infections ◽  
Necrosis Factor Alpha ◽  
Fat Depots ◽  
Necrosis Factor

Cachectin/tumor necrosis factor-alpha (TNF), a protein produced by macrophages upon stimulation, has been implicated as an important mediator of inflammatory processes and of clinical manifestations in chronic infectious diseases. In order to study further the potential role of TNF in infectious diseases, a homologous system was employed in which recombinant Escherichia coli (E. coli) derived bovine TNF (rBoTNF) was injected in cattle, either as a single bolus or in a repetitive treatment-regime. No clinical signs were observed, although changes occurred in hematologic and immunologic parameters when less than 0.5 mg of TNF/100 kg body weight was administered twice daily for 18 days. Prolonged treatment with 0.05–0.5 mg/100 kg induced histologic but no gross changes in the kidneys and liver. When doses were increased above 0.5 mg/100 kg, depression, anorexia, cachexia, and diarrhea appeared rapidly. Pathologic changes were apparent in various tissues including liver, kidneys, and lymphoid organs; body fat depots were depleted. Most of these changes appeared to be reversible; return to normal tissue-morphology occurred within 3 weeks of withdrawal of rBoTNF. The clinical and pathologic changes induced by prolonged rBoTNF administration resembled those observed in some chronic parasitic and viral infections of cattle in which macrophage-activation characteristically occur. Our finding may be relevant to the elucidation of the pathogenesis of these and other chronic infections.

scholarly journals Effects on leukocytes after injection of tumor necrosis factor into healthy humans

Blood ◽  
1992 ◽  
Vol 79 (3) ◽  
pp. 693-698 ◽  
Author(s):  
T van der Poll ◽  
SJ van Deventer ◽  
CE Hack ◽  
GJ Wolbink ◽  
LA Aarden ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Plasma Concentrations ◽  
White Blood Cells ◽  
Controlled Study ◽  
Invasive Infection ◽  
Monocyte Activation ◽  
Healthy Humans ◽  
Septic Syndrome ◽  
Necrosis Factor

Tumor necrosis factor (TNF) has been implicated as a proximal mediator of the septic syndrome. To evaluate the possible role of TNF in leukocyte activation in septicemia, we performed a cross-over saline- controlled study in six healthy men who were intravenously injected with recombinant human TNF (50 micrograms/m2), and analyzed changes in circulating white blood cells and parameters for neutrophil and monocyte activation. TNF elicited a very rapid neutropenia, reaching a nadir after 15 minutes, followed by a neutrophilia. Lymphocytes showed a sustained decrease, whereas monocytes declined transiently. TNF injection was also associated with neutrophil activation, as reflected by a mean fivefold increase in the plasma concentrations of elastase- alpha 1-antitrypsin complexes and a mean sevenfold increase in plasma lactoferrin levels. Serum neopterin, a marker of monocyte activation, was significantly increased 24 hours after the administration of TNF. These changes occurred in the absence of detectable complement activation, as indicated by unchanged C3a-desarg plasma values. Serum interleukin-6 showed a nearly 40-fold increase after TNF injection, whereas interleukin-1 remained undetectable throughout. We conclude that the systemic release of TNF, triggered early after invasive infection, may be involved in the alterations in circulating leukocyte numbers and in the activation of leukocytes, during the development of the septic syndrome.

scholarly journals Granulomatous Infectious Diseases Associated with Tumor Necrosis Factor Antagonists

2004 ◽  
Vol 38 (9) ◽  
pp. 1261-1265 ◽  
Author(s):  
R. S. Wallis ◽  
M. S. Broder ◽  
J. Y. Wong ◽  
M. E. Hanson ◽  
D. O. Beenhouwer
Keyword(s):  
Tumor Necrosis Factor ◽  
Infectious Diseases ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Antagonists ◽  
Necrosis Factor

scholarly journals Effects on leukocytes after injection of tumor necrosis factor into healthy humans

Blood ◽  
1992 ◽  
Vol 79 (3) ◽  
pp. 693-698 ◽  
Author(s):  
T van der Poll ◽  
SJ van Deventer ◽  
CE Hack ◽  
GJ Wolbink ◽  
LA Aarden ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Plasma Concentrations ◽  
White Blood Cells ◽  
Controlled Study ◽  
Invasive Infection ◽  
Monocyte Activation ◽  
Healthy Humans ◽  
Septic Syndrome ◽  
Necrosis Factor

Abstract Tumor necrosis factor (TNF) has been implicated as a proximal mediator of the septic syndrome. To evaluate the possible role of TNF in leukocyte activation in septicemia, we performed a cross-over saline- controlled study in six healthy men who were intravenously injected with recombinant human TNF (50 micrograms/m2), and analyzed changes in circulating white blood cells and parameters for neutrophil and monocyte activation. TNF elicited a very rapid neutropenia, reaching a nadir after 15 minutes, followed by a neutrophilia. Lymphocytes showed a sustained decrease, whereas monocytes declined transiently. TNF injection was also associated with neutrophil activation, as reflected by a mean fivefold increase in the plasma concentrations of elastase- alpha 1-antitrypsin complexes and a mean sevenfold increase in plasma lactoferrin levels. Serum neopterin, a marker of monocyte activation, was significantly increased 24 hours after the administration of TNF. These changes occurred in the absence of detectable complement activation, as indicated by unchanged C3a-desarg plasma values. Serum interleukin-6 showed a nearly 40-fold increase after TNF injection, whereas interleukin-1 remained undetectable throughout. We conclude that the systemic release of TNF, triggered early after invasive infection, may be involved in the alterations in circulating leukocyte numbers and in the activation of leukocytes, during the development of the septic syndrome.

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