The role of adrenal function on the acute phase response to interleukin-1 and tumor necrosis factor

1987 ◽  
Vol 6 ◽  
pp. 53
Keyword(s):  
Tumor Necrosis Factor ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Adrenal Function ◽  
Phase Response ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor, Interleukin 6, and the Acute Phase Response Following Hepatic Ischemia/Reperfusion

1993 ◽  
Vol 55 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Kenneth R. McCurry ◽  
Darrell A. Campbell ◽  
Wendy E. Scales ◽  
Jeffrey S. Warren ◽  
Daniel G. Remick
Keyword(s):  
Tumor Necrosis Factor ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Response ◽  
Tumor Necrosis ◽  
Ischemia Reperfusion ◽  
Phase Response ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Necrosis Factor

scholarly journals Monocyte-conditioned medium, interleukin-1, and tumor necrosis factor stimulate the acute phase response in human hepatoma cells in vitro.

1986 ◽  
Vol 103 (3) ◽  
pp. 787-793 ◽  
Author(s):  
G J Darlington ◽  
D R Wilson ◽  
L B Lachman
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Phase Response ◽  
Human Hepatoma Cells ◽  
The Third ◽  
Necrosis Factor ◽  
Third Component Of Complement

Human hepatoma cells mimic the acute phase response after treatment with monocyte-conditioned medium. Levels of secreted fibrinogen, alpha-1 acid glycoprotein, C-reactive protein, haptoglobin, and the third component of complement were elevated compared with control levels after 48 h of incubation with conditioned supernatant medium from an enriched fraction of normal peripheral monocytes. Albumin levels declined and alpha-1 antitrypsin remained unchanged. Levels of specific mRNA were measured by hybridization to slot blots and Northern blots and changed in correspondence with protein alterations. Interleukin-1 and tumor necrosis factor stimulated the third component of complement, but did not elevate any other member of the acute phase group and were therefore only partially active in this system. The identification of an in vitro model of the human acute phase response will permit analysis of the molecular basis for coordinate regulation of this group of facultative genes.

Interleukin 1-induced depression of iron and zinc: role of granulocytes and lactoferrin

1987 ◽  
Vol 252 (1) ◽  
pp. E27-E32 ◽  
Author(s):  
S. E. Goldblum ◽  
D. A. Cohen ◽  
M. Jay ◽  
C. J. McClain
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Interleukin 1 ◽  
Phase Response ◽  
Human Transferrin ◽  
Carrier Molecule ◽  
Iron And Zinc

The mechanism(s) of stress-induced hypoferremia and hypozincemia remains unclear. We studied the role of granulocytes and lactoferrin (LF) in endotoxin and murine interleukin 1 (IL-1)-induced depression of serum Fe and Zn concentrations in both rabbits and rats. Both endotoxin and IL-1 administration induced significant hypoferremia (P less than 0.01) and hypozincemia (P less than 0.01) after 6 h in both species. Granulocyte depletion before IL-1 infusion significantly (P less than 0.01) diminished the hypoferremia but not the hypozincemia. Moreover, infusion of 5 or 15 mg of human LF into rabbits caused significant hypoferremia (P less than 0.005) without hypozincemia. Significant hypozincemia (P less than 0.01) could only be demonstrated after a 75-mg infusion. In contrast, infusions of human transferrin at equivalent doses (5, 15, and 75 mg) induced neither hypoferremia nor hypozincemia. Therefore endotoxin and IL-1-induced hypoferremia and, to a much lesser degree, hypozincemia are granulocyte dependent. Granulocyte released LF is a specific carrier molecule for transport and removal of Fe from the circulation during the acute phase response. The data suggest a mechanistic dissociation of IL-1-induced hypoferremia and hypozincemia with LF-independent mechanisms for Zn.

Hormonal and metabolic response to recombinant human tumor necrosis factor in rat: in vitro and in vivo

1988 ◽  
Vol 255 (2) ◽  
pp. E206-E212
Author(s):  
R. S. Warren ◽  
H. F. Starnes ◽  
N. Alcock ◽  
S. Calvano ◽  
M. F. Brennan
Keyword(s):  
Tumor Necrosis Factor ◽  
Trace Metal ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Tumor Necrosis ◽  
Metabolic Response ◽  
Zinc Transport ◽  
Necrosis Factor

Tumor necrosis factor (TNF; cachectin) has been implicated as a mediator of the toxic manifestations of overwhelming bacterial infection as well as the chronic catabolic state of cancer cachexia. We have examined the acute metabolic and hormonal response after administration of recombinant human TNF in the rat. TNF given by intraperitoneal injection produced dose- and time-related increases in hepatic amino acid uptake, decreases in serum trace metal concentrations, and a pattern of endocrine hormone alterations characteristic of the acute phase response to tissue injury. In vitro zinc transport studies by rat hepatocytes cultured in the presence of TNF alone, or in combination with recombinant human interleukin 1, another mediator of the acute phase response, demonstrated that neither monokine was capable of directly stimulating zinc transport into cells. These findings suggest that TNF may function as an endogenous mediator of the early metabolic response to sepsis and that the trace metal changes induced by TNF in vivo may occur through a secondary mechanism.

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