Acute-phase behavior of factor VIII procoagulant and other acute-phase reactants in rabbits

1989 ◽  
Vol 257 (1) ◽  
pp. R49-R56
Author(s):  
D. A. Noe ◽  
P. A. Murphy ◽  
W. R. Bell ◽  
J. N. Siegel
Keyword(s):  
Factor Viii ◽  
Acute Phase ◽  
Interleukin 1 ◽  
Plasma Concentrations ◽  
Acute Phase Reactant ◽  
Acute Phase Reactants ◽  
Reactive Protein ◽  
Phase Reactant ◽  
The Mean ◽  
Laboratory Models

We measured the plasma concentrations of factor VIII procoagulant (FVIII:C) in rabbits in two laboratory models of inflammation and after injections of purified homologous interleukin 1 (IL-1). The mean FVIII:C activities 2-4 days following the intramuscular injection of turpentine were significantly elevated, as were the concentrations of fibrinogen and C-reactive protein (CRP). By contrast, rabbits given 50 ng of bacterial lipopolysaccharide intravenously developed increased levels of FVIII:C but not of fibrinogen or CRP. We then studied plasma levels of FVIII:C, fibrinogen, and CRP after injections of either form of purified rabbit IL-1. If the rabbits' temperatures were monitored, FVIII:C levels increased in a log dose-related manner. This effect was not seen unless the rabbits were restrained and was seen in restrained rabbits even if the temperatures were not monitored. Fibrinogen and CRP levels did not change after IL-1 injections. These findings demonstrate that FVIII:C is an acute-phase reactant as judged by its response to turpentine inflammation or endotoxin injections, and to injections of IL-1 in restrained rabbits. FVIII:C appears to be a more sensitive acute-phase reactant than either fibrinogen or CRP. Neither of the latter proteins responded to low-dose endotoxin injections nor to either form of purified homologous IL-1. The doses of IL-1 given did cause fever, neutrophil leukocytosis, and hypoferremia.

scholarly journals Association Between Osteoarticular Scores and Acute Phase Reactant Levels in Rheumatoid Arthritis

2009 ◽  
Vol 28 (2) ◽  
pp. 116-121 ◽  
Author(s):  
Irena Kafeđiska ◽  
Dejan Spasovski ◽  
Todor Gruev ◽  
Mane Grličkov ◽  
Kočo Cakalaroski ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Acute Phase ◽  
Acute Phase Reactant ◽  
Control Group ◽  
Time Intervals ◽  
Acute Phase Reactants ◽  
Mean Values ◽  
Cell Counts ◽  
Phase Reactant ◽  
The Mean

Association Between Osteoarticular Scores and Acute Phase Reactant Levels in Rheumatoid Arthritis The aim of this prospective control study was a quantitative evaluation of the activity of rheumatoid arthritis (RA) in certain time intervals, using articular indexes (set of 28 sensitive and 28 swollen joints), laboratory parameters (Hb, Hct, Er, Le and Plt) and acute phase reactants (ESR, RF, CRP); to determine which of the acute phase reactants is the most useful biochemical marker for the evaluation of disease activity in RA; to quantify the therapeutical and laboratory differences in certain time intervals in the group with and without immunomodulatory therapy with Methotrexate. Sixty patients with RA were included, 27 of who were treated with non-steroid antiinflammatory drugs (NSAIDs) and Methotrexate (MTX). The control group consisted of 33 patients treated only with NSAIDs because of irregular controls. In the first group of patients the disease activity was estimated at four time intervals, and in the control group of patients at three time intervals following the scores of the articular indexes, blood cell counts, ESR and CRP in every patient. In the first group of patients decreased activity of RA was found upon every following control with a consecutive decrease in mean values of the scores of articular indexes with statistically significant differences at the four time intervals. Considering laboratory parameters, there were statistically significant differences in the mean values of Hb, Er, Plt, ESR, (p=0.0462, p=0.0076, p= 0.0058, p= 0.0003). Mean values of CRP did not show statistically significant differences, but the number of patients who were CRP negative increased (there were great standard deviations). In the group of patients treated only with NSAIDs, there were statistically significant differences in the mean values of the scores of articular indexes with an increse at every following control (in favour of progression of the disease). There were no statistically significant differences considering blood cell counts, ESR and CRP (in favour of permanently active disease). In conclusion, CRP is the most useful marker for the prospective follow-up of patients with RA.

scholarly journals Cloning and tissue-specific expression of the gene for mouse C-reactive protein

1993 ◽  
Vol 295 (2) ◽  
pp. 379-386 ◽  
Author(s):  
N O Ku ◽  
R F Mortensen
Keyword(s):  
Acute Phase ◽  
Transcriptional Start Site ◽  
Interleukin 1 ◽  
Acute Phase Reactant ◽  
C Reactive Protein ◽  
Specific Expression ◽  
Tissue Specific ◽  
Tissue Specific Expression ◽  
Reactive Protein ◽  
Phase Reactant

C-reactive protein is a serum acute-phase reactant that increases several thousand-fold in concentration during inflammation in most mammals. However, mouse C-reactive protein is considered to be a minor acute-phase reactant, since its blood level increases only from approx. 0.1 to 1-2 micrograms/ml. A mouse genomic clone of approximately 5 kb was obtained to determine the molecular basis for the regulation of the expression of mouse C-reactive protein. Several cis-acting elements in the 5′ flanking region that potentially regulate transcription were identified: two glucocorticoid-responsive elements, two CCAAT-enhancer-binding protein C (C/EBP) consensus elements that are required for the interleukin-1 responsiveness of some acute-phase reactant genes, an interleukin-6-responsive element, two hepatocyte nuclear factor-1 (HNF-1) elements and a single heat-shock element. Transfection of the hepatoma cell line Hep 3B.2 with a pCAT expression vector containing the 5′ flanking sequence from -1083 to -3 bp from the transcriptional start site, and truncations of this sequence, localized elements that control the tissue-specific expression of mouse C-reactive protein to the two HNF-1 elements and a C/EBP, interleukin-1-responsive element located between -220 and -153, and -90 and -50 bp from the transcriptional start site. A constitutive nuclear protein from mouse-liver hepatocytes specifically binds to the HNF-1 elements. These findings explain the tissue-specific expression of the gene, as well as its limited expression during the acute-phase response.

scholarly journals Mouse C-reactive protein. Generation of cDNA clones, structural analysis, and induction of mRNA during inflammation

1990 ◽  
Vol 266 (1) ◽  
pp. 283-290 ◽  
Author(s):  
A S Whitehead ◽  
K Zahedi ◽  
M Rits ◽  
R F Mortensen ◽  
J M Lelias
Keyword(s):  
Acute Phase ◽  
Acute Phase Reactant ◽  
Untranslated Regions ◽  
Leader Peptide ◽  
Cdna Clones ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Phase Reactant ◽  
Inflammatory Stimuli ◽  
A Minor

A full-length C-reactive protein (CRP) cDNA clone has been isolated from a CBA/J-strain-mouse acute-phase liver library. The 1614-nucleotide cDNA specifies mRNA 5′ and 3′ untranslated regions of 81 and 858 bases respectively that flank 675 bases encoding mouse pre-CRP. The derived amino acid sequence predicts a 19-residue leader peptide followed by a 206-residue mature mouse CRP that shows considerable sequence identity with both human and rabbit CRP. Northern-blot analysis of mouse liver CRP mRNA concentrations after inflammatory stimuli and comparison with hepatic induction of mRNA for the major mouse acute-phase protein serum amyloid P component established that CRP, a major acute-phase reactant in human and rabbit, is a minor acute-phase reactant in mouse. The size and organization of the mouse CRP mRNA 5′ and 3′ untranslated regions are significantly different from those of human and rabbit CRP mRNA and may have implications for its anomalous minimal induction during acute inflammation.

PROTEIN C ACTS AS AN ACUTE PHASE REACTANT IN EQUINE LAMINITIS

1987 ◽  
Author(s):  
K W Prasse ◽  
J N Moore ◽  
A Duncan
Keyword(s):  
Acute Phase ◽  
Protein C ◽  
Coagulation Factors ◽  
Acute Phase Reactant ◽  
Normal Range ◽  
Microvascular Damage ◽  
Acute Phase Reactants ◽  
Intravascular Thrombosis ◽  
Phase Reactant ◽  
Equine Colic

Equine Colic Syndrome is a disease of horses whose complications include laminatis.This term describes a situation where microvascular damage to the hoof causes degeneration of the interphalangeal laminae,leading to lameness. Vascular studies have suggested that microthrombosis involving the delicate vessels in the hoof,coupled with changes in the platelet count, coagulation factors & elevated FDP's implicate DIC as a potential etiology. Limited test capability in the horse has limited further evaluation of this hypothesis. We have developed an assay for equine protein C activity,our normal range being 70-60% (Mean+/- 2SD). We studied 12 horses with the disease for 5 consecutive days,drawing 1 blood sample per day. Our expectation was that protein C levels would decrease.if DIC was significant,as would be expected in humans. No significant decrease was noted in any horse. However there was a significant increase in the protein C levels beyond the upper limit of the normal range in 10 of the 12 horses by the third day. Five of the 10 horses maintained this elevation beyond the 5th day. Thus protein C changes were more consistent with an acute phase reactant response,rather than reflecting the decrease we anicipated,if the equine DIC parallels human DIC. We are measuring other acute phase reactants to see if equine protein C parallels those. Since our assay is still being evaluated,more data needs to be obtained in this and other equine disease states before any definative role for protein C in equine pathology can be determined. In our laminitis horses,we are devolping assays for antithrombin III and plasminogen which should allow us to evaluate the disease state more completley for any involement of elements of intravascular thrombosis and fibrinolysis in the equine colic syndrome.

scholarly journals Platelet agonist synergism by the acute phase reactant C-reactive protein

Blood ◽  
1985 ◽  
Vol 65 (2) ◽  
pp. 264-269
Author(s):  
BA Fiedel
Keyword(s):  
Acute Phase ◽  
Creatine Phosphokinase ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Creatine Phosphate ◽  
Acute Phase Reactant ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Phase Reactant ◽  
Irreversible Aggregation

C-reactive protein is the prototypic acute phase reactant. A self- complexed form (H-CRP) can induce isolated platelets to undergo aggregation, secretion of dense and alpha-granule constituents, and generation of thromboxane A2, but fails to function in platelet-rich plasma (PRP) as a direct agonist. In contrast, when PRP was activated with an amount of adenosine diphosphate (ADP) that produced only reversible platelet aggregation, the presence of H-CRP resulted in irreversible aggregation and the secretion of adenosine triphosphate (ATP). Following a maximum stimulus with ADP alone, where platelet secretion occurred late during the aggregation response, the presence of H-CRP shifted and increased the secretory burst to a time simultaneous with the onset of aggregation. This hypersecretion required H-CRP to be present prior to platelet stimulation or to be added within 15 to 30 seconds following the addition of ADP. H-CRP also potentiated platelet activation stimulated with epinephrine, thrombin, and collagen. When the synergism generated in PRP by H-CRP in the presence of ADP or epinephrine was compared to the synergism similarly produced by aggregated human IgG, collagen, or thrombin, it more closely resembled that of collagen, as reflected by the kinetics and characteristics of synergism and sensitivity to creatine phosphate/creatine phosphokinase or 5,8,11,14-eicosatetraynoic acid. These data provide a philosophically ideal niche for the acute phase (and C-reactive protein) in that a platelet-directed activity associated with this acute phase reactant is not utilized unless platelets are otherwise challenged.

scholarly journals Platelet agonist synergism by the acute phase reactant C-reactive protein

Blood ◽  
1985 ◽  
Vol 65 (2) ◽  
pp. 264-269 ◽  
Author(s):  
BA Fiedel
Keyword(s):  
Acute Phase ◽  
Creatine Phosphokinase ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Creatine Phosphate ◽  
Acute Phase Reactant ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Phase Reactant ◽  
Irreversible Aggregation

Abstract C-reactive protein is the prototypic acute phase reactant. A self- complexed form (H-CRP) can induce isolated platelets to undergo aggregation, secretion of dense and alpha-granule constituents, and generation of thromboxane A2, but fails to function in platelet-rich plasma (PRP) as a direct agonist. In contrast, when PRP was activated with an amount of adenosine diphosphate (ADP) that produced only reversible platelet aggregation, the presence of H-CRP resulted in irreversible aggregation and the secretion of adenosine triphosphate (ATP). Following a maximum stimulus with ADP alone, where platelet secretion occurred late during the aggregation response, the presence of H-CRP shifted and increased the secretory burst to a time simultaneous with the onset of aggregation. This hypersecretion required H-CRP to be present prior to platelet stimulation or to be added within 15 to 30 seconds following the addition of ADP. H-CRP also potentiated platelet activation stimulated with epinephrine, thrombin, and collagen. When the synergism generated in PRP by H-CRP in the presence of ADP or epinephrine was compared to the synergism similarly produced by aggregated human IgG, collagen, or thrombin, it more closely resembled that of collagen, as reflected by the kinetics and characteristics of synergism and sensitivity to creatine phosphate/creatine phosphokinase or 5,8,11,14-eicosatetraynoic acid. These data provide a philosophically ideal niche for the acute phase (and C-reactive protein) in that a platelet-directed activity associated with this acute phase reactant is not utilized unless platelets are otherwise challenged.

scholarly journals Murine serum glycoprotein gp70 behaves as an acute phase reactant.

1982 ◽  
Vol 155 (2) ◽  
pp. 345-357 ◽  
Author(s):  
I Hara ◽  
S Izui ◽  
F J Dixon
Keyword(s):  
T Cells ◽  
Acute Phase ◽  
Viral Genome ◽  
Lipid A ◽  
Acute Phase Reactant ◽  
Acute Phase Reactants ◽  
Single Intraperitoneal Injection ◽  
Phase Reactant ◽  
Immunohistochemical Studies ◽  
Parenchymal Cells

A single intraperitoneal injection of bacterial lipopolysaccharide (LPS) or its lipid A component induced high levels of glycoprotein, gp70, in sera of several strains of mice within 24 h. This serum gp70 response induced by LPS was independent of the activation of B cells and the presence of T cells. However, serological and immunohistochemical studies demonstrated the production of gp70 by hepatic parenchymal cells and its subsequent release into the circulating blood. The expression of gp70 in the serum was enhanced not only by LPS but also other inducers of acute phase reactants (APR) such as turpentine oil or polyriboinosinic-polyribocytidylic acid. Further, the serum gp70 response was kinetically identical to those of APR. These results strongly suggest that (a) the liver may be the major source for serum gp70, (b) serum gp70 behaves like an APR, (c) its expression may be controlled by a mechanism similar to that for other APR, and (d) this glycoprotein apparently behaves as a normal host constituent and not a product of a viral genome.

scholarly journals Binding of fibronectin by the acute phase reactant C-reactive protein.

1984 ◽  
Vol 259 (3) ◽  
pp. 1496-1501 ◽  
Author(s):  
E M Salonen ◽  
T Vartio ◽  
K Hedman ◽  
A Vaheri
Keyword(s):  
Acute Phase ◽  
Acute Phase Reactant ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Phase Reactant

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.

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