Associations of erythrocyte membrane fatty acids with the concentrations of C-reactive protein, interleukin 1 receptor antagonist and adiponectin in 1373 men

2014 ◽  
Vol 91 (4) ◽  
pp. 169-174 ◽  
Author(s):  
M.J. Takkunen ◽  
V.D.F. de Mello ◽  
U.S. Schwab ◽  
J.J. Ågren ◽  
J. Kuusisto ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Receptor Antagonist ◽  
Erythrocyte Membrane ◽  
Interleukin 1 ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Membrane Fatty Acids ◽  
Interleukin 1 Receptor Antagonist

scholarly journals Association of C-Reactive Protein, Interleukin-1 Receptor Antagonist and Adiponectin with the Metabolic Syndrome

2007 ◽  
Vol 2007 ◽  
pp. 1-8 ◽  
Author(s):  
Juha Saltevo ◽  
Mauno Vanhala ◽  
Hannu Kautiainen ◽  
Esko Kumpusalo ◽  
Markku Laakso
Keyword(s):  
Metabolic Syndrome ◽  
Receptor Antagonist ◽  
Interleukin 1 ◽  
High Sensitivity ◽  
Population Based ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Interleukin 1 Receptor Antagonist ◽  
The Metabolic Syndrome ◽  
Hs Crp

This Finnish population-based study, mean age 46 years, evaluates the association of high-sensitivity C-reactive protein (hs-CRP), interleukin-1 receptor antagonist (IL-1Ra), and adiponectin with the NCEP and IDF definitions of metabolic syndrome (MetS). Adiponectin levels were higher, hs-CRP and IL-1Ra levels lower in subjects without MetS compared to subjects with MetS. If MetS was present according to both IDF and NCEP criteria, BMI, waist, triglycerides, hs-CRP, and IL-1Ra were significantly higher compared to subjects who had MetS according to either only IDF or only NCEP criteria. The hs-CRP, IL-1Ra, and adiponectin linearly correlated with the number of the components of MetS according to both definitions. Decreased levels of adiponectin and increased levels of hs-CRP and IL-1Ra are tightly associated with the components of MetS. Individuals who had MetS according to both criteria had the most adverse changes in cardiovascular risk factors.

HIGH ALTITUDE INCREASES CIRCULATING INTERLEUKIN-6, INTERLEUKIN-1 RECEPTOR ANTAGONIST AND C-REACTIVE PROTEIN

Cytokine ◽  
2000 ◽  
Vol 12 (3) ◽  
pp. 246-252 ◽  
Author(s):  
G. Hartmann ◽  
M. Tschöp ◽  
R. Fischer ◽  
C. Bidlingmaier ◽  
R. Riepl ◽  
...  
Keyword(s):  
High Altitude ◽  
Receptor Antagonist ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Interleukin 1 Receptor Antagonist

Interleukin-4 (IL-4) and IL-13 Enhance the Effect of IL-1β on Production of IL-1 Receptor Antagonist by Human Primary Hepatocytes and Hepatoma HepG2 Cells: Differential Effect on C-Reactive Protein Production

Blood ◽  
1999 ◽  
Vol 93 (4) ◽  
pp. 1299-1307
Author(s):  
Cem Gabay ◽  
Brandon Porter ◽  
Denis Guenette ◽  
Bahri Billir ◽  
William P. Arend
Keyword(s):  
Receptor Antagonist ◽  
Hepg2 Cells ◽  
Messenger Rna ◽  
Interleukin 1 ◽  
Interleukin 4 ◽  
C Reactive Protein ◽  
Primary Hepatocytes ◽  
Human Hepatoma Cells ◽  
Reactive Protein ◽  
Human Primary Hepatocytes

Interleukin-1 receptor antagonist (IL-1Ra) is produced by hepatocytes with characteristics of an acute-phase protein. To examine the role of IL-4 and IL-13 in production of IL-1Ra, human primary hepatocytes and HepG2 human hepatoma cells were cultured in the presence of IL-4 or IL-13 in combination with IL-1β and/or IL-6. The results indicated that both IL-4 and IL-13 amplified the stimulatory effect of IL-1β on production of IL-1Ra protein and messenger RNA (mRNA) by both human primary hepatocytes and HepG2 cells. IL-1Ra refers to three different peptides, one secreted (sIL-1Ra) and two intracellular (icIL-1RaI and icIL-1RaII), derived from the same gene. sIL-1Ra and icIL-1RaI are the products of two different mRNA, whereas icIL-1RaII is synthesized by alternative translation initiation mainly from sIL-1Ra mRNA. Our results show that both sIL-1Ra and icIL-1RaII, but not icIL-1RaI, are produced by HepG2 cells and human hepatocytes. Transient transfection experiments as well as mRNA stability studies indicated that IL-4 stimulated sIL-1Ra production primarly at the level of transcription. Gel retardation assays showed that IL-4 induced the formation of a STAT6-DNA complex with a STAT6 binding element within the sIL-1Ra promoter, but had no effect on IL-1–induced NF-κB binding activity. In contrast to IL-1Ra, production of C-reactive protein by human primary hepatocytes was stimulated by IL-6 and decreased by the addition of IL-4.

Sign in / Sign up

Export Citation Format

Share Document