Effects of protein malnutrition on IL-6-mediated signaling in the liver and the systemic acute-phase response in rats

2004 ◽  
Vol 287 (4) ◽  
pp. R801-R808 ◽  
Author(s):  
Pei-Ra Ling ◽  
Robert J. Smith ◽  
Susanne Kie ◽  
Patricia Boyce ◽  
Bruce R. Bistrian
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Levels ◽  
Protein Malnutrition ◽  
Phase Response ◽  
Low Grade ◽  
Signaling Proteins ◽  
Protein Group ◽  
Liver Changes ◽  
Related Proteins

This study examines the effects of malnutrition on IL-6 signaling pathways of rats fed 2% vs. 20% casein diets for 14 days. Effects of malnutrition on the abundance and IL-6-stimulated phosphorylation of signaling proteins in the JAK-STAT and MAP kinase pathways were examined in the liver. Changes of the acute-phase response as reflected by serum α1-acid glycoprotein (AG), TNF-α (TNF), and IL-1β (IL-1) were compared in the two dietary groups at 0, 4, 8, 16, and 24 h after IL-6 administration. Under basal conditions, the abundance of the IL-6 receptor, gp130, JAK1, STAT1, and STAT3 proteins and levels of phosphorylation of ERK1/2 and p38 were significantly increased in the liver in the 2% casein group compared with the 20% casein group. With IL-6 stimulation, the increased phosphorylation per unit of protein of these signaling proteins was not different in the liver between the two groups. Before IL-6 stimulation, serum levels of TNF, IL-1, IL-6, and AG were significantly higher in the 2% casein group than in the 20% casein group. After bolus injection of IL-6, changes in IL-1 and AG were similar in the two dietary groups, although a slight decline in AG level was noted after 8 h of IL-6 administration in the 2% protein group. These data demonstrate that protein malnutrition produces changes in inflammation-related proteins characteristic of a low-grade systemic inflammatory response and, thus, can serve as an inflammatory stimulus. The capacity for response to IL-6 is preserved, suggesting adaptive preservation of acute-phase responsiveness during malnutrition.

Transient decreased retinol serum levels in children with pneumonia and acute phase response

2011 ◽  
Author(s):  
Kellen C. K. Barbosa ◽  
Daniel F. Cunha ◽  
Alceu A. Jordão Jr. ◽  
Virgínia R. S. Weffort ◽  
Selma F. C. Cunha
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Levels ◽  
Phase Response

Acute phase response after myocardial infarction: Correlation between serum levels of cytokines and C-reactive protein

1990 ◽  
Vol 68 (21) ◽  
pp. 1083-1083 ◽  
Author(s):  
H. Tilg ◽  
J. Mair ◽  
M. Herold ◽  
W. E. Aulitzky ◽  
P. Lechleitner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Levels ◽  
Phase Response ◽  
C Reactive Protein ◽  
Reactive Protein

Evidence that brief stress may induce the acute phase response in rats

1997 ◽  
Vol 273 (6) ◽  
pp. R1998-R2004 ◽  
Author(s):  
Terrence Deak ◽  
Jennifer L. Meriwether ◽  
Monika Fleshner ◽  
Robert L. Spencer ◽  
Amer Abouhamze ◽  
...  
Keyword(s):  
Body Temperature ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Core Body Temperature ◽  
Serum Levels ◽  
Phase Response ◽  
Single Session ◽  
Acid Glycoprotein ◽  
Corticosteroid Binding Globulin ◽  
Core Body

Exposing rats to a single session of inescapable tail shock (IS) reduces corticosteroid binding globulin (CBG) 24 h later (Fleshner et al., Endocrinology 136: 5336–5342, 1995). The present experiments examined whether reductions in CBG are differentially affected by controllable vs. identical uncontrollable tail shock, are mediated by IS-induced glucocorticoid elevation, or reflect IS-induced activation of the acute phase response and whether IS produces fever. The results demonstrate that 1) equivalent reductions in CBG are observed in response to escapable tail shock or yoked IS, 2) IS-induced CBG reduction is not blocked by adrenalectomy in rats that receive basal corticosteroid replacement or by pretreatment with RU-38486, and 3) IS appears to activate the acute phase response, since IS reduces serum levels of an acute-phase negative reactant (CBG), increases serum levels of acute-phase positive reactants (haptoglobin and α1-acid glycoprotein), and increases core body temperature 20–24 h later.

The relationship between serum levels of lipoprotein(a) and proteins associated with the acute phase response

1993 ◽  
Vol 223 (1-2) ◽  
pp. 73-82 ◽  
Author(s):  
Thomas B. Ledue ◽  
Louis M. Neveux ◽  
Glenn E. Palomaki ◽  
Robert F. Ritchie ◽  
Wendy Y. Craig
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Levels ◽  
Phase Response ◽  
Lipoprotein A ◽  
The Relationship

Association Between Stent Implantation and Progression of Nontarget Lesions in a Rabbit Model of Atherosclerosis

2021 ◽  
Author(s):  
Jing Ma ◽  
Xiaoling Liu ◽  
Lei Qiao ◽  
Linlin Meng ◽  
Xingli Xu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Acute Phase ◽  
Systemic Inflammation ◽  
Stent Implantation ◽  
Acute Phase Response ◽  
Rabbit Model ◽  
Serum Levels ◽  
Phase Response ◽  
Plaque Burden ◽  
Amyloid A

Background: Progression of nontarget lesions (NTLs) after percutaneous coronary intervention (PCI) has been reported. However, it remains unknown whether progression of NTLs was causally related to stenting. This study was undertaken to test the hypothesis that stent implantation triggers acute phase response and systemic inflammation which may be associated with progression of NTLs. Methods: Thirty New Zealand rabbits receiving endothelial denudation and atherogenic diet were randomly divided into stenting, sham, and control groups. Angiography and intravascular ultrasonography were performed in the stenting and sham groups, and stent implantation performed only in the stenting group. Histopathologic study was conducted and serum levels of APPs (acute phase proteins) measured in all rabbits. Proteomics analysis was performed to screen the potential proteins related to NTLs progression after stent implantation. The serum levels of APPs and inflammatory cytokines were measured in 147 patients undergoing coronary angiography or PCI. Results: Plaque burden in the NTLs was significantly increased 12 weeks after stent implantation in the stenting group versus sham group. Serum levels of APPs and their protein expression in NTLs were significantly increased and responsible for stenting-triggered inflammation. In patients receiving PCI, serum levels of SAA-1 (serum amyloid A protein 1), CRP (C-reactive protein), TNF (tumor necrosis factor)-α, and IL (interleukin)-6 were substantially elevated up to 1 month post-PCI. Conclusions: In a rabbit model of atherosclerosis, stent implantation triggered acute phase response and systemic inflammation, which was associated with increased plaque burden and pathological features of unstable plaque in NTLs. The potential mechanism involved vessel injury-triggered acute phase response manifested as increased serum levels of SAA-1, CRP, and LBP (lipopolysaccharide-binding protein) and their protein expression in NTLs. These findings provided a new insight into the relation between stent implantation and progression of NTLs, and further studies are warranted to clarify the detailed mechanism and clinical significance of these preliminary results. REGISTRATION: URL: http://www.chictr.org.cn ; Unique identifier: ChiCTR1900026393.

Glycoprotein biosynthesis during the acute-phase response to inflammation

1983 ◽  
Vol 61 (9) ◽  
pp. 1041-1048 ◽  
Author(s):  
J. C. Jamieson ◽  
H. A. Kaplan ◽  
B. M. R. N. J. Woloski ◽  
M. Hellman ◽  
K. Ham
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Elevated Serum ◽  
Serum Cortisol ◽  
Serum Levels ◽  
Acute Phase Reactant ◽  
Phase Response ◽  
Acute Phase Reactants ◽  
Acid Glycoprotein ◽  
Phase Reactant

Inflammation results in an increase in the levels of a variety of glycoproteins in serum. The glycoproteins that respond in this way are usually referred to as acute-phase reactants. Studies on the acute-phase response of rat α1-acid glycoprotein showed that there was an increase in the liver levels of this glycoprotein at 12 h after turpentine inflammation. This was followed by increased serum levels at 48–72 h after inflammation, suggesting a precursor–product relationship between liver and serum α1-acid glycoprotein. Incorporation studies coupled with measurements of synthesis rates of α1-acid glycoprotein showed that increased synthesis was responsible for the acute-phase response of this protein to inflammation. These studies also showed that albumin was a negative acute-phase reactant. The acute-phase response of α1-acid glycoprotein was accompanied by increased liver pools of UDP–N-acetylglucosamine (UDP–GlcNAc) and UDP–N-acetylgalactosamine (UDP–GalNAc) and increased liver activities of glucosamine-6-phosphate synthase and UDP–GlcNAc 2-epimerase. Activities of galactosyl and sialyl transferases in liver were also elevated and serum sialyl transferase was increased substantially in inflammation, suggesting that it may also be an acute-phase reactant. Liver activities of β-N-acetylhexosaminidase and β-galactosidase declined by about 50% at 24 h after inflammation; there was evidence that serum levels of these enzymes increased at 24–72 h after inflammation, suggesting that the lysosomal glycosidases may be released from liver during inflammation. Inflammation resulted in elevated serum Cortisol, insulin, and adrenocorticotropic hormone and induced increased glycogenosis; liver cAMP levels were also increased during inflammation. Preliminary studies are presented to show that leukocyte-derived factors may be involved in the acute-phase response of α1-acid glycoprotein to inflammation.

The Acute-phase Response Is Not Predictive for the Development of Arthritis in Seropositive Arthralgia – A Prospective Cohort Study

2012 ◽  
Vol 39 (10) ◽  
pp. 1914-1917 ◽  
Author(s):  
MAARTEN LIMPER ◽  
LOTTE van de STADT ◽  
WOUTER BOS ◽  
MARTIJN de KRUIF ◽  
ARNOLD SPEK ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Messenger Rna ◽  
Immunoglobulin M ◽  
Phase Response ◽  
Low Grade ◽  
Baseline Serum ◽  
Tnf Α ◽  
Clinical Arthritis

Objective.To evaluate whether markers of the acute-phase response in patients presenting with arthralgia and positive anticitrullinated protein antibodies (ACPA) and/or immunoglobulin M rheumatoid factor (IgM-RF) could be predictive for the development of arthritis.Methods.In total, 137 ACPA- and/or IgM-RF-positive patients were included. Patients were followed annually for the development of arthritis, defined as presence of 1 or more swollen joints at clinical examination. High-sensitivity C-reactive protein (hsCRP), procalcitonin (PCT), secretory phospholipase A2 (SPLA2), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), IL-12p70, IL-10, and interferon-γ (IFN-γ) were measured in baseline serum samples. Gene expression focusing on a predefined panel of genes coding for inflammatory molecules was measured by multiplex ligation-dependent probe amplification.Results.Thirty-five patients (26%) developed arthritis within a median time of 11 months (interquartile range 3.7–18 mo). Circulating levels of cytokines, SPLA2, hsCRP, and PCT were not different between patients with progression to clinical arthritis and those without progression. However, a trend for IL-12p70, TNF-α, IL-10, IL-6, and SPLA2 was observed. No correlation between messenger RNA (mRNA) expression levels of inflammatory genes and progression to arthritis was found. Subgroup analysis of patients with early progression to arthritis showed higher levels of mRNA expression of poly(A)-specific ribonuclease and polycomb complex protein BMI-1 compared to patients without progression to arthritis.Conclusion.Although low-grade inflammation is present before onset of clinical arthritis in large cohorts and can be detected using consecutive measurements, a single measurement of acute-phase reactants seems to have limited value for prediction of development of arthritis in individual patients.

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