scholarly journals Induction of interleukin-1 and interleukin-1 receptor antagonist during contaminated in-vitro dialysis with whole blood

1996 ◽  
Vol 11 (1) ◽  
pp. 101-108 ◽  
Author(s):  
R. Schindler ◽  
S. Krautzig ◽  
V. Lufft ◽  
G. Lonnemann ◽  
A. Mahiout ◽  
...  
1996 ◽  
Vol 11 (1) ◽  
pp. 101-108 ◽  
Author(s):  
R. Schindler ◽  
S. Krautzig ◽  
V. Lufft ◽  
G. Lonnemann ◽  
A. Mahiout ◽  
...  

2019 ◽  
Vol 47 (8) ◽  
pp. 1955-1963 ◽  
Author(s):  
Sean M. Muir ◽  
Natalie Reisbig ◽  
Michael Baria ◽  
Christopher Kaeding ◽  
Alicia L. Bertone

Background: Currently, platelet-poor plasma (PPP) is a discarded waste product of platelet-rich plasma (PRP) and may contain valuable proteins. Purpose/Hypothesis: The study’s goal was to evaluate the concentration of plasma as a potential additive biotherapy for the treatment of osteoarthritis. We hypothesized that a novel polyacrylamide concentration device would efficiently concentrate insulin-like growth factor–1 (IGF-1) from PPP and be additive to PRP or autologous protein solution (APS). Study Design: Descriptive laboratory study. Methods: A laboratory study was conducted with human and equine whole blood from healthy volunteers/donors. Fresh samples of blood and plasma were processed and characterized for platelet, white blood cell, and growth factor/cytokine content and then quantified by enzyme-linked immunosorbent assays specific for IGF-1, transforming growth factor–β, interleukin-1β, and interleukin-1 receptor antagonist as representatives of cartilage anabolic and inflammatory mediators. Results: A potent cartilage anabolic protein, IGF-1, was significantly concentrated by the polyacrylamide concentration device in both human and equine PPP. The polyacrylamide device also substantially increased plasma proteins over whole blood, most dramatically key proteins relevant to the treatment of osteoarthritis, including transforming growth factor–β (29-fold over blood) and interleukin-1 receptor antagonist (70-fold over plasma). Conclusion: Concentrated PPP is a unique source for biologically relevant concentrations of IGF-1. PRP and APS can produce greater concentrations of other anabolic and anti-inflammatory proteins not found in plasma. Clinical Relevance: The polyacrylamide device efficiently concentrated PPP to create a unique source of IGF-1 that may supplement orthopaedic biologic therapies.


1992 ◽  
Vol 42 (6) ◽  
pp. 1419-1424 ◽  
Author(s):  
Brian J.G. Pereira ◽  
Debra D. Poutsiaka ◽  
Andrew J. King ◽  
James A. Strom ◽  
Geetha Narayan ◽  
...  

1994 ◽  
Vol 50 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Mitsuhiro Tada ◽  
Annie-Claire Diserens ◽  
Isabelle Desbaillets ◽  
Rehana Jaufeerally ◽  
Marie-France Hamou ◽  
...  

2020 ◽  
Vol 02 (02) ◽  
pp. e109-e116
Author(s):  
Ying Zheng ◽  
Xinyi Xiao ◽  
Zhuoyi Yang ◽  
Meiqi Zhou ◽  
Hui Chen ◽  
...  

AbstractInterleukin-1 receptor antagonist is an important acute-phase protein and an immune mediator, and its expression is associated with the development of hepatitis or acute liver failure. The aim of this study was to investigate whether recombinant human interleukin-1 receptor antagonist directly targets and improves cell survival in a carbon tetrachloride-induced hepatocyte injury model in vitro. A human hepatoma cell line and a mouse hepatocyte cell line were used to establish carbon tetrachloride-induced cell injury models in vitro, and cell viability, apoptosis, and reactive oxygen species level were determined to assess the degree of hepatocellular damage. Quantitative real-time polymerase chain reaction was used to analyze the level of interleukin-1β, interleukin-6, and tumor necrosis factor-α mRNA in cells; extracellular regulated protein kinases 1/2 phosphorylation in hepatocytes was analyzed using western blotting. Recombinant human interleukin-1 receptor antagonist could directly target hepatocytes, improve cell survival, and decrease carbon tetrachloride-induced cell apoptosis in vitro. In hepatocytes, recombinant human interleukin-1 receptor antagonist remarkably downregulated expression of interleukin-1β, interleukin-6, and tumor necrosis factor-α in hepatocytes exposed to carbon tetrachloride. It also decreased accumulation of reactive oxygen species and abrogated the suppression of extracellular regulated protein kinases 1/2 phosphorylation induced by carbon tetrachloride. However, stimulation of cells with an extracellular regulated protein kinases 1/2 inhibitor blocked the recombinant human interleukin-1 receptor antagonist-induced upregulation of extracellular regulated protein kinase1/2 activation and abrogated the improvement in hepatocyte survival following carbon tetrachloride treatment. Collectively, these findings provide new insights into the hepatocyte-protective mechanism of recombinant human interleukin-1 receptor antagonist.


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