scholarly journals Release of cytokines, soluble cytokine receptors, and interleukin-1 receptor antagonist after intravenous immunoglobulin administration in vivo

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2136-2143 ◽  
Author(s):  
P Aukrust ◽  
SS Froland ◽  
NB Liabakk ◽  
F Muller ◽  
I Nordoy ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Intravenous Immunoglobulin ◽  
Plasma Levels ◽  
Interleukin 1 ◽  
Cytokine Receptors ◽  
Tnf Alpha ◽  
Ivig Infusion ◽  
Molar Excess ◽  
Interleukin 1 Receptor Antagonist

Abstract We investigated the in vivo effects of one bolus injection (400 mg/kg) of intravenous immunoglobulin (IVIG) on a number of cytokines, soluble cytokine receptors, and interleukin-1 receptor antagonist (IL-1Ra) in plasma in 12 patients with primary hypogammaglobulinemia. A significant and rapid increase in plasma levels of IL-6, IL-8, and tumor necrosis factor alpha (TNF alpha) was seen within 1 hour after IVIG infusion. This increase was accompanied by a more prolonged elevation in levels of both types of soluble TNF receptors (sTNFRs), which remained elevated throughout the study period (44 hours) although they reached peak levels within 1 hour. After an initial increase in the ratio between TNF alpha and sTNFRs, this ratio decreased to values significantly lower than baseline values 20 and 44 hours postinfusion with approximately 600-fold molar excess of sTNFRs to TNF alpha (trimer). Although only a modest but statistically significant increase in plasma levels of IL-1 beta was seen, IVIG infusion was followed by a marked increase in plasma levels of IL-1Ra with 1,000-fold molar excess of IL-1Ra to IL-1 beta in some patients. The demonstrated effects of IVIG infusion on the cytokine network, particularly the induction of IL- 1Ra and sTNFRs release, might be important for the therapeutic effects of IVIG in several immune-mediated disorders.

scholarly journals Release of cytokines, soluble cytokine receptors, and interleukin-1 receptor antagonist after intravenous immunoglobulin administration in vivo

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2136-2143 ◽  
Author(s):  
P Aukrust ◽  
SS Froland ◽  
NB Liabakk ◽  
F Muller ◽  
I Nordoy ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Intravenous Immunoglobulin ◽  
Plasma Levels ◽  
Interleukin 1 ◽  
Cytokine Receptors ◽  
Tnf Alpha ◽  
Ivig Infusion ◽  
Molar Excess ◽  
Interleukin 1 Receptor Antagonist

We investigated the in vivo effects of one bolus injection (400 mg/kg) of intravenous immunoglobulin (IVIG) on a number of cytokines, soluble cytokine receptors, and interleukin-1 receptor antagonist (IL-1Ra) in plasma in 12 patients with primary hypogammaglobulinemia. A significant and rapid increase in plasma levels of IL-6, IL-8, and tumor necrosis factor alpha (TNF alpha) was seen within 1 hour after IVIG infusion. This increase was accompanied by a more prolonged elevation in levels of both types of soluble TNF receptors (sTNFRs), which remained elevated throughout the study period (44 hours) although they reached peak levels within 1 hour. After an initial increase in the ratio between TNF alpha and sTNFRs, this ratio decreased to values significantly lower than baseline values 20 and 44 hours postinfusion with approximately 600-fold molar excess of sTNFRs to TNF alpha (trimer). Although only a modest but statistically significant increase in plasma levels of IL-1 beta was seen, IVIG infusion was followed by a marked increase in plasma levels of IL-1Ra with 1,000-fold molar excess of IL-1Ra to IL-1 beta in some patients. The demonstrated effects of IVIG infusion on the cytokine network, particularly the induction of IL- 1Ra and sTNFRs release, might be important for the therapeutic effects of IVIG in several immune-mediated disorders.

scholarly journals Ultrasound Biomicroscopic Imaging for Interleukin-1 Receptor Antagonist–Inhibiting Atherosclerosis and Markers of Inflammation in Atherosclerotic Development in Apolipoprotein-E Knockout Mice

2015 ◽  
Vol 42 (4) ◽  
pp. 319-326 ◽  
Author(s):  
Rong-Juan Li ◽  
Yan Sun ◽  
Qin Wang ◽  
Jiao Yang ◽  
Ya Yang ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Receptor Antagonist ◽  
Plasma Levels ◽  
Interleukin 1 ◽  
Age Groups ◽  
Ultrasound Biomicroscopy ◽  
Interleukin 1 Receptor Antagonist ◽  
Markers Of Inflammation ◽  
Apolipoprotein E Knockout Mice

We sought to validate the hypothesis that the development of atherosclerosis can be suppressed by the interleukin-1 receptor antagonist (IL-1Ra) in murine models of atherosclerosis in vivo, noninvasively seen by means of high-resolution ultrasound biomicroscopy, and we studied changes in inflammatory markers such as IL-1 and C-reactive protein (CRP) plasma levels in these models of atherosclerosis. We divided IL-1Ra+/−/apolipoprotein-E (apoE)−/− and IL-1Ra+/+/apoE−/− mice into 2 age groups, used as atherosclerotic models. The control groups were age-matched IL-1Ra+/+/apoE+/+ mice. Plaque thickness was measured in the ascending aorta in short-axis images by means of ultrasound and histology. Plasma levels of IL-1 and CRP were quantified in the 3 murine groups. At 16 weeks, plaque thickness in the ascending aortas of the IL-1Ra+/−/apoE−/− mice was significantly greater than that in the IL-1Ra+/+/apoE−/− mice, on ultrasound and histology (P <0.01). In contrast, at 32 weeks, the differences between these 2 genotypes were not statistically significant. Serum IL-1 levels were lower in the IL-1Ra+/−/apoE−/− mice than in the IL-1Ra+/+/apoE−/− mice at 16 and 32 weeks (P <0.05). At 16 weeks, serum CRP levels in the IL-1Ra+/−/apoE−/− mice were higher than in the IL-1Ra+/+/apoE−/− mice (P <0.01). Our results suggest that ultrasound biomicroscopy enables evaluation of atherosclerotic lesions in vivo, noninvasively and in real-time, in apoE−/− mice. Partial IL-1Ra deficiencies might promote early plaque development in 16-week-old apoE−/− mice. The balance of IL-1 and IL-1Ra might influence atherosclerotic development. Finally, CRP might affect the initiation of atherosclerosis, rather than its progression.

Microparticles Locally Deliver Active Interleukin-1 Receptor Antagonist In Vivo

2018 ◽  
Vol 7 (16) ◽  
pp. 1800263 ◽  
Author(s):  
Anna E. B. Clements ◽  
Emily R. Groves ◽  
Connie S. Chamberlain ◽  
Ray Vanderby ◽  
William L. Murphy
Keyword(s):  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Interleukin 1 Receptor Antagonist

In vivo suppression of early experimental osteoarthritis by interleukin-1 receptor antagonist using gene therapy

1997 ◽  
Vol 40 (6) ◽  
pp. 1012-1019 ◽  
Author(s):  
Jean-Pierre Pelletier ◽  
John P. Caron ◽  
Christopher Evans ◽  
Paul D. Robbins ◽  
Helga I. Georgescu ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Interleukin 1 Receptor Antagonist ◽  
Experimental Osteoarthritis

scholarly journals Effect of interleukin-1 (IL-1) blockade on cytokine synthesis: I. IL-1 receptor antagonist inhibits IL-1-induced cytokine synthesis and blocks the binding of IL-1 to its type II receptor on human monocytes

Blood ◽  
1992 ◽  
Vol 79 (9) ◽  
pp. 2356-2363 ◽  
Author(s):  
EV Granowitz ◽  
BD Clark ◽  
E Vannier ◽  
MV Callahan ◽  
CA Dinarello
Keyword(s):  
Receptor Antagonist ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Tnf Alpha ◽  
Type Ii ◽  
Human Monocytes ◽  
Molar Excess ◽  
Cytokine Synthesis

Interleukin-1 (IL-1) induces IL-1, tumor necrosis factor alpha (TNF alpha), and IL-6 gene expression and synthesis in a variety of cells. In this study, we investigated the ability of human recombinant IL-1 receptor antagonist (IL-1ra) to inhibit IL-1-induced cytokine production in human peripheral blood mononuclear cells (PBMC) and isolated monocytes. IL-1ra alone at concentrations as high as 1 microgram/mL did not induce IL-1 alpha, IL-1 beta, TNF alpha, or IL-6 synthesis. Suppression of IL-1-induced IL-1, TNF alpha, or IL-6 synthesis was dose-dependent (P less than or equal to .0001). At a twofold molar excess, IL-1ra inhibited IL-1-induced IL-1 or TNF alpha synthesis by 50% (P less than .01); an equimolar concentration of IL- 1ra inhibited synthesis of these two cytokines by over 20% (P less than .05). A 10-fold molar excess of IL-1ra over IL-1 beta reduced IL-1 beta- induced IL-1 alpha by 95% (P = .01) and IL-1 alpha-induced IL-1 beta by 73% (P less than .01). IL-1ra added to PBMC 8 hours after stimulation with IL-1 beta was still able to inhibit IL-1 alpha, TNF alpha, and IL- 6 synthesis (P less than or equal to .01). A similar reduction in IL-1 beta-induced IL-1 alpha was observed when IL-1 beta was removed from the cultures after 8 hours of stimulation (P less than .05), suggesting a prolonged presence of IL-1 or restimulation of IL-1 receptors on monocytes is required for the induction of cytokines. In elutriated monocytes, a 10-fold molar excess of IL-1ra reduced IL-1 beta-induced IL-1 alpha by 82% (P less than .05), TNF alpha by 64% (P = .05), and IL- 6 by 47% (P less than .05). 125I-IL-1 beta was bound to purified monocytes, cross-linked, and immunoprecipitated. Sodium dodecyl sulfate- polyacrylamide gel electrophoresis showed a band at 85 Kd corresponding to the 68-Kd IL-1 receptor type II (IL-1RtII). Excess unlabeled IL-1 beta or IL-1ra blocked the binding of 125I-IL-1 beta to the IL-1RtII. We conclude that IL-1ra inhibits IL-1-induced cytokine synthesis and competes with IL-1 for the IL-1RtII on human monocytes.

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