Acute Phase Proteins and Interleukin?6 Serum Levels in Patients with Chronic Arterial Occlusion

2006 ◽  
Vol 762 (1) ◽  
pp. 493-495 ◽  
Author(s):  
WACLAW MAJEWSKI ◽  
RYSZARD STANISZEWSKI ◽  
ARTUR SLUPIANEK ◽  
ALEKSANDER GORNY ◽  
ANDRZEJ MACKIEWICZ
Keyword(s):  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Arterial Occlusion ◽  
Serum Levels ◽  
Chronic Arterial Occlusion

scholarly journals Immunoreactive interleukin-6 and acute phase proteins as prognostic factors in multiple myeloma. Finnish Leukemia Group

Blood ◽  
1995 ◽  
Vol 85 (3) ◽  
pp. 765-771 ◽  
Author(s):  
TT Pelliniemi ◽  
K Irjala ◽  
K Mattila ◽  
K Pulkki ◽  
A Rajamaki ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Regression Analysis ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Clinical Stage ◽  
Prognostic Significance ◽  
Serum Levels ◽  
High Serum ◽  
Bone Lesions

High serum level of bioactive interleukin-6 (IL-6) is regarded as a predictor of poor prognosis in multiple myeloma (MM). On the other hand, the reported levels of immunoreactive IL-6 have been highly variable, and the prognostic value of immunoreactive IL-6 in MM is not clear. We have analyzed the prognostic significance of serum immunoreactive IL-6, as measured by a sensitive immunosorbent assay, in 210 patients with newly diagnosed MM subsequently treated with intermittent melphalan and prednisone. The serum levels of acute phase proteins C-reactive protein (CRP), alpha 1-antitrypsin (alpha 1AT), and acid alpha 1-glycoprotein (orosomucoid; OM) were evaluated as surrogates for IL-6. Serum IL-6, CRP, alpha 1AT, and OM levels were raised in 42%, 40%, 41%, and 24% of the patients, respectively. There was a significant correlation between the clinical stage of the patients and serum IL-6 (P = .006), alpha 1AT (P = .001), and OM (P = .004) levels at diagnosis. At 3 years, 52% of the patients were alive. Univariate logistic regression analysis showed that high levels of IL-6 (P = .002), CRP (P = .02), alpha 1AT (P < .001), OM (P = .007), beta 2- microglobulin (beta 2M; P < .001), and thymidine kinase (P < .05) were all associated with 3-year mortality. In multivariate regression analysis, beta 2M (P < .0001) and alpha 1AT (P = .01) had independent prognostic significance. The patients with high levels of both beta 2M and alpha 1AT or IL-6 were at very high risk of dying within 3 years from diagnosis (16% and 21% of the patients in these groups were alive, respectively). When the patients were stratified according to the clinical stage, the prognostic significance of serum IL-6 and alpha 1AT was especially evident in stage II patients. When the patients were divided into two groups according to normal or raised serum IL-6 levels, the patients with high IL-6 levels had more frequent osteolytic bone lesions (P = .03) and a more aggressive disease. We conclude that serum immunoreactive IL-6 is a significant prognostic marker in MM.

Synergistic action of interleukin-6 and glucocorticoids is mediated by the interleukin-6 response element of the rat alpha 2 macroglobulin gene

1992 ◽  
Vol 12 (5) ◽  
pp. 2282-2294
Author(s):  
G M Hocke ◽  
D Barry ◽  
G H Fey
Keyword(s):  
Dna Binding ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Binding Proteins ◽  
Nuclear Dna ◽  
Acute Phase Proteins ◽  
Dna Binding Proteins ◽  
Human Hepatoma Cells ◽  
Response Element ◽  
Multiple Copies

One class of genes coding for the acute-phase proteins (acute-phase genes) is induced by interleukin 6 (IL-6) through the human transcription factor NF-IL-6 and its rat homolog IL-6-DBP/LAP. A second class, represented by the rat alpha 2 macroglobulin gene, utilizes a different IL-6 response element (IL-6-RE) and different DNA-binding proteins interacting with this element, the so-called IL-6-RE binding proteins (IL-6 RE-BPs). Human Hep3B and HepG2 hepatoma, U266 myeloma, and CESS lymphoblastoid cells contain IL-6 RE-BPs that form complexes, with the IL-6-RE, with gel mobilities indistinguishable from those of the corresponding complexes of rat liver cells. The ability to form these complexes was induced by IL-6 in human hepatoma cells with a maximum reached after 4 h and required ongoing protein synthesis. Multiple copies of an 18-bp element containing the IL-6-RE core were sufficient to confer both induction by IL-6 and a synergistic induction by IL-6 plus glucocorticoids to minimal promoters. The synergism was blocked by the receptor antagonist RU486 and thus was dependent on the glucocorticoid receptor (GR). However, the 18-bp element contained no consensus GR-binding site, and recombinant GR did not bind at this sequence. Therefore, the synergism was probably achieved by an indirect effect of a glucocorticoid-activated intermediate gene on the IL-6 RE-BPs. The rat IL-6 RE-BP had a molecular weight of 102 +/- 10 kDa and was thus distinct from NF-IL-6 and IL-6-DBP/LAP. Therefore, IL-6 must activate two different classes of liver acute-phase genes through at least two different nuclear DNA-binding proteins: NF-IL-6/IL-6-DBP/LAP and the IL-6 RE-BP.

Abstract 1629: Genetic Polymorphism A1675G On Angiotensin Receptor Type 2, Is Implicated In The Expression Of Acute Phase Proteins And The Development Of Coronary Atherosclerosis In Hypertensive Patients

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Dimitris Tousoulis ◽  
Nikolas Koumallos ◽  
Charalambos Antoniades ◽  
Despina Kardara ◽  
Alexis S Antonopoulos ◽  
...  
Keyword(s):  
Genetic Polymorphism ◽  
Arterial Hypertension ◽  
Acute Phase ◽  
Coronary Atherosclerosis ◽  
Acute Phase Proteins ◽  
Renin Angiotensin System ◽  
Serum Levels ◽  
Hypertensive Patients ◽  
The Impact

Introduction: Renin-angiotensin system affects cardiovascular disease pathogenesis through a balance of angiotensin II effects on proatherogenic constitutive type 1 and antiatherogenic inducible type 2 (AT2R) receptors. The impact of A1675G polymorphism on the development of hypertension and advanced atherosclerosis is controversial. We examined the impact of A1675G polymorphism on AT2R, on the risk for arterial hypertension and coronary atherosclerosis, and its effect on the expression of proatherogenic inflammatory molecules. Methods. The study population consisted of 310 males: 145 with arterial hypertension and 165 controls, matched for age and risk factors for atherosclerosis. Among hypertensive subjects, 37 had angiographically documented coronary atherosclerosis and 108 had no evidence of atherosclerosis. The presence of A1675G polymorphism on AT2R gene (located in chromosome X) was determined by PCR. Serum levels of C-reactive protein and fibrinogen was measured in all the participants. Results. The frequency of the A allele was similar between patients with arterial hypertension (64/145, 44.1%) and non-hypertensive subjects (73/165, 44.2%, p=NS), while the risk for arterial hypertension was OR[95%CI]:1.004[0.641–1.574], p=0.985 for the G vs A carriers. However, the risk for coronary atherosclerosis within the group of hypertensive subjects was significantly elevated in the carriers of the A allele (OR[95%CI]:2.128[1.003–4.513], p=0.04 vs carriers of the G allele). Importantly, the presence of the A allele was also associated with significantly higher levels of CRP (4.8±0.8mg/dl) compared to the carriers of the G allele (3.0±0.3mg/dl, p<0.05). Similarly, fibrinogen levels were higher in A-allele carriers (median(25 th –75th percentile) 395(340 – 455) mg/ml) compared to G-allele carriers (369(320 – 406) mg/ml, p<0.05). Conclusions: Although genetic polymorphism A1675G on AT2R is not associated with the development of arterial hypertension, it affects the risk for coronary artery disease among hypertensive patients. The presence of the A allele also leads to higher levels of CRP and fibrinogen, implying that this polymorphism may induce atherogenesis by modulating acute phase response in hypertensive individuals.

scholarly journals Recombinant human interleukin-6 (IL-6/BSF-2/HSF) regulates the synthesis of acute phase proteins in human hepatocytes

FEBS Letters ◽  
1988 ◽  
Vol 232 (2) ◽  
pp. 347-350 ◽  
Author(s):  
José V. Castell ◽  
Maria J. Gómez-Lechón ◽  
Martina David ◽  
Toshio Hirano ◽  
Tadamitsu Kishimoto ◽  
...  
Keyword(s):  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Human Hepatocytes

scholarly journals Pathogenic significance of interleukin-6 (IL-6/BSF-2) in Castleman's disease

Blood ◽  
1989 ◽  
Vol 74 (4) ◽  
pp. 1360-1367 ◽  
Author(s):  
K Yoshizaki ◽  
T Matsuda ◽  
N Nishimoto ◽  
T Kuritani ◽  
L Taeho ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Nodes ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Castleman’S Disease ◽  
Germinal Centers ◽  
Surgical Removal ◽  
Castleman's Disease ◽  
Lymph Node Hyperplasia

Abstract Castleman's disease is a syndrome consisting of giant lymph node hyperplasia with plasma cell infiltration, fever, anemia, hypergammaglobulinemia, and an increase in the plasma level of acute phase proteins. It has been reported that clinical abnormalities disappear after the resection of the affected lymph nodes, suggesting that products of lymph nodes may cause such clinical abnormalities. Interleukin-6 (IL-6) is a cytokine inducing B-cell differentiation to immunoglobulin-producing cells and regulating biosynthesis of acute phase proteins. This report demonstrates that the germinal centers of hyperplastic lymph nodes of patients with Castleman's disease produce large quantities of IL-6 without any significant production of other cytokines. In a patient with a solitary hyperplastic lymph node, clinical improvement and decrease in serum IL-6 were observed following surgical removal of the involved lymph node. There was a correlation between serum IL-6 level, lymph node hyperplasia, hypergammaglobulinemia, increased level of acute phase proteins, and clinical abnormalities. The findings in this report indicate that the generation of IL-6 by B cells in germinal centers of hyperplastic lymph nodes of Castleman's disease may be the key element responsible for the variety of clinical symptoms in this disease.

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