Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum and bone marrow from 21 patients with rheumatoid arthritis (RA) were studied in order to establish the pathogenetic role of interleukin-6 (IL-6) in anemia of chronic disease (ACD). Erythroid colony growth, using burst forming units of erythroblasts (BFUe) as a parameter, was impaired in ACD and not in nonanemic RA controls. Serum IL-6 was elevated in ACD and it correlated well with parameters of disease activity such as erythrocyte sedimentation rate and C-reactive protein. IL-6 addition to bone marrow cultures had inconsistent effects while anti-IL-6 addition resulted in impaired erythroid colony growth, suggesting stimulatory effects of IL-6 produced in the medium, which may be masked by simultaneous production of cytokines with suppressive effects. It was concluded that elevated serum IL-6 in ACD reflects disease activity. It probably plays no pathogenetic role in ACD. Its stimulatory effects on erythroid growth might counteract suppressive effects of other interleukins.
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PMID:Anaemia of chronic disease in rheumatoid arthritis. Raised serum interleukin-6 (IL-6) levels and effects of IL-6 and anti-IL-6 on in vitro erythropoiesis. 239 39

The three monokines interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), and interleukin-6 (IL-6) modulate acute phase plasma protein synthesis in adult human hepatocytes. Only IL-6 stimulates the synthesis of the full spectrum of acute phase proteins as seen in inflammatory states in humans, i.e. synthesis and secretion of C-reactive protein, serum amyloid A, fibrinogen, alpha 1-antitrypsin, alpha 1-antichymotrypsin and haptoglobin are increased while albumin, transferrin and fibronectin are decreased. IL-1 beta as well as TNF alpha, although having a moderate effect on the positive acute phase proteins and inhibiting the synthesis of fibrinogen, albumin and transferrin, fail to induce serum amyloid A and C-reactive protein. These data suggest that IL-6 plays the key role in the regulation of acute phase protein synthesis in human hepatocytes.
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PMID:Interleukin-6 is the major regulator of acute phase protein synthesis in adult human hepatocytes. 246 4

One of the mediators responsible for the induction of the production of acute phase proteins by hepatocytes is interleukin-6 (IL-6), formally known as hybridoma growth factor (HGF). In a prospective study the biological significance of IL-6, but also the relationship with the acute phase response (C-reactive protein [CRP], alpha 1-antitrypsin and alpha 1-acid glycoprotein) during flare-ups in 12 systemic lupus erythematosus (SLE) patients was investigated. Only 2 SLE patients showed sustained elevated IL-6 levels, and in one of these patients a clear correlation was found between the increases in IL-6 and the acute phase response. In the other SLE patients hardly any response or change in the levels of IL-6, CRP, and/or alpha 1-antitrypsin was found. In contrast to the profiles of alpha 1-acid glycoprotein, in seven of the SLE patients a significant increase in the serum levels took place in the period preceding the exacerbation. This difference between the three acute phase proteins suggests that the regulatory mechanisms are different. Our results are in agreement with the findings that IL-6 might be responsible for the CRP response.
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PMID:Interleukin-6 (IL-6) and acute phase proteins in the disease course of patients with systemic lupus erythematosus. 247 Dec 49

In the rodent, the general response to acute inflammation and tissue damage is characterized by a complex rearrangement in the pattern of concentrations of proteins in the plasma leading to an increase in the sedimentation rate of erythrocytes, an increase in leukocyte concentration in the bloodstream, and a decrease in the hematocrit. Body temperature changes only slightly or not at all. The reasons for the change in plasma concentrations of proteins are changes in their rates of synthesis in the liver. Degradation of plasma proteins is not affected. The details of the acute phase response evolved in the interaction of species with their environment. Therefore, it is not surprising to find differences in the details of the acute phase response among species. For example, alpha 2-macroglobulin is a strongly positive acute phase reactant in the rat, but not in the mouse; C-reactive protein is a strongly positive acute phase protein in the mouse, but is not found in the rat. An inducible acute phase cysteine proteinase inhibitor system, which has evolved from a primordial kininogen gene, has been observed so far only in the rat. The changes in the synthesis rates of acute phase proteins during inflammation are closely reflected by corresponding changes in intracellular mRNA levels. In the liver, the capacity to induce the acute phase pattern of synthesis and secretion of plasma proteins probably develops around birth. Changes in mRNA levels are brought about by changes in transcription rates or by changes in mRNA stability. Kinetics of mRNA changes during the acute phase response differ for individual proteins. The main signal compound for eliciting the acute phase response in liver seems to be interleukin-6/interferon-beta 2/hepatocyte stimulating factor, whereas interleukin-1 leads to typical acute phase changes in mRNA levels only for alpha 1-acid glycoprotein, albumin, and transthyretin. Plasma protein genes are expressed in various extrahepatic tissues, such as the choroid plexus, the yolk sac, the placenta, the seminal vesicles, and other sites. All these tissues are involved in maintaining protein homeostasis in associated extracellular compartments by synthesis and secretion of proteins. Synthesis and secretion of plasma proteins in paracompartmental organs other than the liver is not influenced by the acute phase stimuli.
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PMID:The acute phase response in the rodent. 247 96

Human C-reactive protein (CRP) is the major acute phase reactant during acute inflammation. The human CRP promoter is expressed in an inducible and cell-specific manner when linked to the bacterial CAT gene and transfected into human hepatoma cell cultures. In this paper we analyze the effect of several recombinant cytokines or CRP promoter inducibility in human Hep3B cells. When cytokines are tested singly the major inducer of CRP-CAT fusions is interleukin-6 (IL-6). Maximal CAT gene expression, however, is only achieved when both interleukin-1 beta (IL-1 beta) and IL-6 are present. The response to the two cytokines is cooperative. Cooperativity is maintained when the CRP promoter is linked to a different coding region, that of the bacterial neomycin phosphotransferase II gene. With a series of 5' and 3' deletions we show the existence of two distinct and independent regions responsive to IL-6 and located upstream to the TATA box. The IL-1 effect is exerted at the level of downstream sequences that are probably important for optimal mRNA translatability or nuclear-cytoplasmic transport. Inducibility is not influenced by the activation of protein kinases C or A and does not require new protein synthesis.
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PMID:Dual control of C-reactive protein gene expression by interleukin-1 and interleukin-6. 255 73

IL-6/IFN-beta 2 is a family of phosphoglycoproteins ranging in size from 19 to 30 kDa which elicits a broad range of physiologic and immune responses. Several cytokines, including TNF, have been shown to stimulate IL-6 production in cell culture. In this report, we describe the rapid induction of circulating biologically active IL-6 by the systemic administration of rTNF to patients with cancer. Low levels of IL-6 activity could be detected in the sera of patients as early as 5 min after rTNF infusion. IL-6 levels peaked approximately 2 to 3 h after rTNF bolus administration and were undetectable in most cases within 8 h. IL-6 was detected in two separate bioassays--the hybridoma B9 proliferation and the hepatocyte-stimulating factor assay. Maximum detectable levels of IL-6 ranged from 160 to 310 hybridoma growth factor units and 11-82 ng/ml in the hepatocyte-stimulating factor assay. IL-6 induction decreased after serial, daily doses of rTNF. Serial serum samples of patients receiving IL-2 or IFN-alpha were also assayed for IL-6 production. IL-2-treated but not IFN-alpha-treated patients generated low levels of IL-6 (range less than 20 to 95 hybridoma growth factor units/ml). Interestingly, in patients treated with IL-2, serum levels of TNF were detectable and peak TNF activity preceded measurable IL-6 levels. Serum levels of acute phase plasma proteins and of corticosteroid rose in response to rTNF administration. C-reactive protein increased (2.5 to 4.0-fold) within 8 h of rTNF administration and cortisol levels rose (10- to 20-fold) within 4 h after rTNF injection. We conclude that rTNF administration in man leads to the induction of circulating IL-6 which, due to its broad range of activities, may be an important physiologic signal regulating the immune response.
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PMID:IL-6/IFN-beta-2 as a circulating hormone. Induction by cytokine administration in humans. 278 45

Interleukin-6 (IL-6), also called 26-kd protein, hybridoma plasmacytoma growth factor, beta 2-interferon, or B cell stimulatory factor 2, is a recently described human cytokine with multiple growth and differentiation activities. Using a very sensitive bioassay based on the growth factor activity of this protein for B cell hybridomas, we found that IL-6 activity was significantly elevated in synovial fluid from patients with rheumatoid arthritis (RA) or other inflammatory arthritides, as compared with that in a group of patients with osteoarthritis. Moreover, IL-6 was detected in about one-third of the serum samples from patients with RA. In the latter group, we found a significant correlation between serum IL-6 activity and serum levels of C-reactive protein, alpha 1-acid glycoprotein, alpha 1-antitrypsin, fibrinogen, and haptoglobin, which indicates that IL-6 is related to disease activity in patients with RA.
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PMID:Interleukin-6 in synovial fluid and serum of patients with rheumatoid arthritis and other inflammatory arthritides. 326 Jan 2

During the acute phase response, synthesis of C-reactive protein and serum amyloid A is increased. To investigate whether the enhanced synthesis of these proteins are due to stimulatory effect of inflammatory mediators such as interleukin-1 (IL-1) and interleukin-6 (IL-6) produced by macrophages and monocytes, primary cultures of adult human hepatocytes were exposed to recombinant (r)IL-1, rIL-6 or rIL-1 and monospecific anti rIL-6 antibodies in the presence of 1 microM dexamethasone. The findings indicate that rIL-1 and rIL-6 both stimulate the liver synthesis of C-reactive protein and serum amyloid A, however monospecific anti rIL-6 antibodies reduce the stimulatory effect of rIL-1 on the synthesis of these proteins. These findings suggest that IL-6 plays a key role in the stimulation of synthesis of serum amyloid A and C-reactive protein by the human liver cells.
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PMID:The effect of interleukin-1, interleukin-6 and its interrelationship on the synthesis of serum amyloid A and C-reactive protein in primary cultures of adult human hepatocytes. 326 80

Interleukin-6 (IL-6) is a monokine with a number of biological activities, which are intimately related to inflammatory responses. We have measured IL-6 levels in synovial fluid (SF) and serum (Se) of patients with rheumatic diseases. SF-IL-6 levels were a thousand-fold higher than corresponding Se levels and a positive correlation was found between SF and Se levels suggesting that Se-IL-6 is derived from IL-6 produced in the joint. Se levels of IL-6 were also positively correlated to C-reactive protein (CRP) levels, supporting the in vitro experiments showing that IL-6 stimulates hepatocytes to produce CRP. Finally we observed a positive correlation between SF-IL-6 levels and the local activity score.
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PMID:Interleukin-6 (IL-6) in synovial fluid and serum of patients with rheumatic diseases. 326 31

Laparoscopic surgery may reduce the inflammatory response to surgery by the avoidance of a skin incision which is frequently the site of maximum tissue trauma. We hypothesized that the inflammatory response is less with minimally invasive procedures. The aim of this study was to evaluate the response of inflammatory mediators following laparoscopic and open hernia repair. Thirty-four patients undergoing unilateral primary inguinal hernia repair were prospectively assigned to either laparoscopic mesh hernia repair (n = 14), open mesh hernia repair (n = 11), or a Bassini repair (n = 9). Serum samples withdrawn prior to surgery, 6 h after surgery, and then again at 24 h after surgery were assayed for interleukin-6 and C-reactive protein content. Interleukin-6 levels at 24 h in the laparoscopic (13.1 +/- 3.1 pg/ml), open mesh (15.5 +/- 2.5 pg/ml), or Bassini group) (15.4 +/- 2.0 pg/ml) did not differ significantly. Neither did C-reactive protein levels at 24 h in the laparoscopic (12.4 +/- 2.7 pg/ml), open mesh (23.0 +/- 7.8 pg/ml), or Bassini group 18.6 +/- 6.6 pg/ml) differ significantly. The response of inflammatory mediators to hernia repair is not modified by undertaking the procedure laparoscopically.
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PMID:Inflammatory markers following laparoscopic and open hernia repair. 748 66


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