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)

Using an aseptic technique, samples of amniotic fluid were obtained from the forewaters and hindwaters of fifteen women in spontaneous labour with a deeply engaged fetal head. Prior to sampling, a cervical swab was obtained to exclude infection and in 10 cases samples of amniotic fluid were sent for microscopy and culture. Forewater samples were obtained using a pudendal block needle. Hindwater samples were obtained after membrane rupture by inserting an intra-uterine pressure catheter. Batch assay for interleukin-6 (IL-6) concentrations was performed using a specific ELISA. The levels of IL-6 in forewater samples of amniotic fluid were significantly higher than those found in hindwater samples (t = 3.65, P < 0.002). This suggests that either the production of IL-6 as a result of stimulation by its cytokine 'effectors' is greater at this site, or that the loss or metabolism of IL-6 in the forewaters is less than that in the hindwaters. The concentration of IL-6 parallels the reported levels of PGE2, and it is therefore likely that if IL-6 is involved in the mechanism of labour it acts through the effects of the resultant PGE2 release.
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PMID:Interleukin-6 in amniotic fluid obtained at forewater amniotomy compared with hindwater samples in women in spontaneous labour. 763 34

This study investigated the effects of feeding mice lipids with different fatty acid compositions upon the ability of stimulated macrophages to produce inflammatory mediators. Weanling mice were fed for 8 weeks on a low-fat (LF; 2.5% by weight) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), or menhaden (fish) oil (MO). Thioglycollate-elicited peritoneal macrophages were isolated. Macrophages isolated from MO-fed mice produced less PGE2, 6-keto-PGF1 alpha, TXB2, and interleukin-6 in response to lipopolysaccharide (LPS) stimulation than those from mice fed each of the other diets. Macrophages from mice fed the OO, SO, or MO diets produced less tumor necrosis factor alpha in response to LPS stimulation than those from mice fed the LF or HCO diets. There was no effect of dietary lipid manipulation upon the production of interleukin-1 by LPS-stimulated macrophages. Macrophages from mice fed the MO diet produced more superoxide and hydrogen peroxide in response to phorbol ester stimulation than those from mice fed each of the other diets. In response to unopsonized zymosan, macrophages from mice fed the SO or MO diets produced more hydrogen peroxide than macrophages from mice fed the other diets. LPS-stimulated nitric oxide production was greater from macrophages from OO-, SO-, or MO-fed mice than from those fed the LF or HCO diets. Thus, the nature of the lipid consumed in the diet has significant effects upon the production of a variety of inflammatory mediators by macrophages. The most potent effect is caused by fish oil consumption. Possible mechanisms by which dietary fatty acids, particularly the n-3 polyunsaturated fatty acids found in fish oils, could affect mediator production by macrophages are described. The clinical relevance of such effects is discussed.
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PMID:Effects of dietary lipid manipulation upon inflammatory mediator production by murine macrophages. 775 22

Protein-energy malnutrition is associated with intrinsic defects in macrophage (MO) microbicidal function, but effects on MO-CD4+ cell interaction are unclear. This study examined the effect of protein-energy malnutrition on components of Ag presentation (AP) by peritoneal macrophages (PMO) and splenocyte responses (MLR) in the naive (resident) and infected state (mycobacterium-BCG), and assessed the potential role of prostaglandin (PGE2) and L-arginine-derived nitric oxide (NO) as regulatory mechanisms in these immune interactions. Mice were randomized to receive either a control (24% casein, RD) or low-protein (2.5% casein, LPD) diets for 8 weeks. PMO and splenocytes were harvested and AP function and MLR assessed +/- NG-mono-methyl-L-arginine (NMMA; competitive inhibitor of NO. synthesis) or indomethacin (PGE2 inhibitor). PMO components of AP were evaluated, including phagocytic function, MHC-class II (Ia) expression, and interleukin-1 (IL-1) and interleukin-6 (IL-6) production. PGE2 production and NO. (measured as NO-2) synthesis were also assessed. AP and MLR were preserved in protein-energy malnutrition in both resident and activated states. BCG infection in RD was associated with PMO activation as measured by increased O-2 and NO-2 release, but impaired AP and MLR responses. NMMA and indomethacin enhanced AP and MLR in RD groups only. Individual components of PMO AP (phagocytosis, IL-1 and IL-6 production) were defective during protein-energy malnutrition, as were NO-2 and PGE2 production. Thus, AP and MLR were preserved in LPD groups which may be related to a loss of prostaglandin- and L-arginine-mediated suppressor mechanisms.
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PMID:Antigen presentation in protein-energy malnutrition. 775 32

Infections, trauma and inflammatory processes induce a host response with increases in a large group of structurally and functionally diverse plasma proteins. Parental administration of foreign proteins also induce an increase in plasma fibrinogen. Interleukin-6 (IL-6) is a monocyte-derived mediator and has regulatory effects on acute phase protein genes which result in the induction of fibrinogen synthesis in primary hepatocytes, while the addition of interleukin-1 (IL-1) exerts a negative modulating influence on the IL-6-stimulated fibrinogen. In order to understand the mechanisms by which IL-1 inhibits IL-6-stimulated fibrinogen transcription and translation, and since IL-1 is believed to act through PGE2 stimulation, we have studied the influence of PGE2 in IL-6 or IL-1, alone and in combination, on Fg mRNA expression (by Northern blot analysis) and the influence of PGE2, indomethacin, and arachidonic acid on Fg secretion. Moreover, since human recombinant interleukin-1 receptor antagonist (hrIL-1ra) is a strong inhibitor of IL-1 induced IL-1 transcription and translation and has an inhibitory effect on PGE2, we have studied the effects of IL-1ra on the down-regulation of IL-6 stimulated fibrinogen by IL-1, using an Fg ELISA method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The down-regulation of IL-6-stimulated fibrinogen steady state mRNA and protein levels by human recombinant IL-1 is not PGE2-dependent: effects of IL-1 receptor antagonist (IL-1RA). 777 69

This review considers the mechanisms controlling collagen deposition in mammalian lung in five different states: normal development, fibrosis, erosion, pneumonectomy, and the steady state. Deposition is the net result of positive and negative processes. The major positive processes are control of cell number and type, regulation of transcription and translation, post-translational modifications, fibril formation, and covalent cross-linking. The negative mechanisms are intracellular degradation, collagenase-mediated degradation, and phagocytosis, and they are integral to the life cycle of collagen. Cytokines and growth factors have many and complex effects on all the processes that constitute collagen metabolism. Interleukin-1 and tumor necrosis factor-alpha can either stimulate or inhibit collagen accumulation, presumably depending on the immediate environment. Interleukin-6 inhibits collagen degradation, and gamma-interferon inhibits collagen production. Platelet derived growth factor and fibroblast growth factor have powerful mitogenic effects on connective tissue cells in lung, and can also affect collagen production directly. Transforming growth factor-beta activates a battery of processes that uniformly contribute to accumulation of collagen. Transforming growth factor-beta may be the "master switch" for a fibrotic program in lung. Therapeutic approaches to controlling lung fibrosis by manipulating cytokine levels are promising. Prostaglandin E has uniformly negative effects on net collagen accumulation and may play a central role in an erosion program.
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PMID:Control of collagen deposition in mammalian lung. 777 Apr 62

Interleukin-6 has a variety of biological effects, mainly on the immune system. The regulation of this signal at both the site of production and the site of action is necessary to maintain the organism's homeostasis. In the microenvironment of the hepatic sinusoids, Kupffer cells as resident macrophages are the most potent source of interleukin-6 during inflammation. This cytokine is an important signal to hepatocytes during the early stages of the acute-phase response, leading to the expression of several major plasma proteins. Kupffer cells were found to express interleukin-6 receptor constitutively. Interleukin-6 decreased the level of interleukin-6 receptor mRNA, indicating an autocrine pathway by which Kupffer cells regulate their responsiveness to interleukin-6. Furthermore, lipopolysaccharide, tumor necrosis factor-alpha, interferon-gamma, interleukin-1 beta and phorbol ester induced interleukin-6 production and, at the same time, suppressed the level of interleukin-6 receptor mRNA. The existence of an autocrine loop in rat Kupffer cells may be physiologically relevant, as it would contribute to a regulated interleukin-6 signal chain in the liver. The anti-inflammatory mediators dexamethasone or PGE2 and its second messenger, cyclic AMP, increased interleukin-6 receptor mRNA, whereas prostaglandin D2 or the Ca2+ ionophore, A 23187, were without effect. The changes in interleukin-6 mRNA were paralleled by the number of interleukin-6 receptors present on Kupffer cells as detected by binding of 125I-interleukin-6. These results suggest the existence of control mechanisms involving several soluble mediators that help balance the level of interleukin-6-R mRNA in rat liver macrophages.
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PMID:Regulation of interleukin-6 receptor expression in rat Kupffer cells: modulation by cytokines, dexamethasone and prostaglandin E2. 781

Interleukin-6 (IL-6) is a multifunctional cytokine that is elevated in vivo during acute infection, chronic inflammation, and some hematopoietic malignancies. To understand how IL-6 becomes elevated in vivo, it is important to identify factors that can stimulate its secretion from effector cells. We found that commercial preparations of bovine serum albumin (BSA) stimulated murine macrophages to secrete high levels of IL-6. In fact, BSA was at least as potent as bacterial lipopolysaccharide (LPS) in stimulating IL-6 production. Stimulation was clearly visible at concentrations as low as 20 micrograms/mL and reached saturation at 0.5 to 1 mg/mL albumin, at which concentration 1.1 x 10(6) oil-elicited macrophages produced 6,000 +/- 700 B9 units of IL-6 in an overnight incubation. Prostaglandin E2 production was induced by the same concentrations of BSA. Both resident and oil-elicited peritoneal cells were responsive to the albumin. The stimulatory activity did not derive from contamination of the protein with Escherichia coli LPS; when compared directly with LPS, the response to BSA was more rapid, had a higher amplitude, and was not inhibitable by polymyxin B. In addition, macrophages isolated from C3H/HeJ mice, which have an inherited defect in their ability to respond to LPS, secreted IL-6 in response to BSA but not to LPS. The stimulatory activity was stable to heat, mild acid, and reduction/alkylation and copurified with albumin on Cibachron Blue agarose (Sigma, St Louis, MO) and anti-albumin immunoaffinity chromatography. Comparison of different sources and preparations of albumin showed differences in the levels of IL-6-inducing activity; three different lots of commercial fatty acid-free BSA and one lot of polymer-enhanced BSA stimulated IL-6 secretion by more than 100-fold over basal levels whereas other preparations showed more limited activity. A sample of BSA that was active in vitro caused a marked elevation of IL-6 when injected into BALB/c mice, thus demonstrating inflammatory activity in vivo. When the albumin preparations were fractionated by ion exchange and gel filtration chromatography and then analyzed by sodium dodecyl sulfate-gel electrophoresis and Western blot immunoassay, it was found that the IL-6-inducing activity resided in high molecular weight polymers of albumin. The ability of albumin polymers to stimulate IL-6 production represents a novel mechanism for modulation of this cytokine.
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PMID:Stimulation of interleukin-6 and prostaglandin E2 secretion from peritoneal macrophages by polymers of albumin. 821 33

Infectious reactions are known to comprise changes in vasopermeability and inflammatory mediators. We used peritonitis that complicated continuous ambulatory peritoneal dialysis (CAPD) as an in vivo inflammation model to study the time courses of peritoneal permeability characteristics and mediators in dialysate. Sixteen episodes of peritonitis were prospectively followed on eight consecutive days from the onset of the infection and once after recovery (control). Dialysate night dwells were examined for marker proteins of peritoneal permeability, cytokines (tumor necrosis factor-alpha [TNF-alpha], interleukin-6 [IL-6] and prostaglandins (PGE2, 6-keto-PGF1 alpha, and thromboxane B2 [TxB2]). The clearance of beta 2-microglobulin was used as indicator of the effective peritoneal surface area. The intrinsic permeability was characterized functionally by the peritoneal restriction coefficient. All protein clearances were increased during the acute phase of peritonitis and subsequently decreased to control. Likewise, the intrinsic peritoneal permeability was elevated, as demonstrated by a decrease of the peritoneal restriction coefficient. Peritoneal appearance rates of TNF-alpha, IL-6, and prostaglandins were also increased during the acute phase. Peak values were reached on day 1. The largest increase was observed for IL-6 (median 854-fold), followed by TNF-alpha (35-fold). The vasodilating PGE2 and 6-keto-PGF1 alpha were increased 12-fold and the vasoconstricting TxB2 was increased threefold. Evidence was obtained for local intraperitoneal synthesis of IL-6 and prostaglandins. TNF-alpha production appeared to be present only during the early acute inflammatory response. Analysis of variance for repeated measurements revealed that changes in the clearance of beta 2-microglobulin were related to those in IL-6 and marginally also to TNF-alpha in dialysate. Changes in the peritoneal restriction coefficient were also related to IL-6, but were more closely related to alterations in dialysate PGE2. These findings suggest that TNF-alpha, IL-6, and PGE2 are involved in the changes in permeability characteristics during CAPD-related peritonitis.
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PMID:Relationship of TNF-alpha, interleukin-6, and prostaglandins to peritoneal permeability for macromolecules during longitudinal follow-up of peritonitis in continuous ambulatory peritoneal dialysis. 824 82

In this study we investigated the effects of the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) on prostaglandin production by cultured human fetal membranes. These cytokines stimulate prostaglandin synthesis by isolated components of human fetal membranes, but their effects on the intact tissue comprising amnion, chorion and decidua were not known. TNF-alpha added to the maternal side of the membrane activated decidual production of PGF2 alpha but had no effects on synthesis of PGE2 or PGE2 metabolites. Addition of TNF-alpha to the fetal side of the membrane increased production of PGE2 by amnion and PGE2 metabolites from chorion. The addition of IL-6 to the fetal or the maternal side of the membrane increased production of PGE2 from amnion and PGE2m from chorion, suggesting that IL-6 might pass through the fetal membrane. IL-6 had no effect on decidual PGF2 alpha production. These results suggest that TNF-alpha may be involved in labor by increasing decidual prostaglandin synthesis, whereas IL-6 is less likely to have a role.
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PMID:Effects of interleukin-6 and tumor necrosis factor-alpha on prostaglandin production by cultured human fetal membranes. 824 48

Interleukin-6 (IL-6) was secreted by cultured cells of 7 out of 11 human pituitary adenomas that were examined. Interleukin-1 (IL-1) stimulated IL-6 release after a 24-h incubation period in five of the seven IL-6-secreting adenoma cultures and in all seven after 72 h. Tumour necrosis factor, interferon-gamma and epidermal growth factor did not significantly affect IL-6 secretion. Interleukin-1 failed to induce measurable IL-6 in the cultures that did not secrete IL-6 under basal conditions. Prostaglandin E2 did not influence basal IL-6 secretion and indomethacin did not inhibit IL-1-stimulated IL-6 release. In addition, pertussis toxin had no effect on IL-1-stimulated IL-6 release. The growth hormone (GH) secretory response to IL-1 varied, with stimulation in one GH-secreting adenoma culture, no significant effect in a second and inhibition in a third. Interleukin-1 did not significantly affect the release of prolactin, thyrotrophin, luteinizing hormone or follicle-stimulating hormone in any of the adenoma cultures. This study provides evidence that IL-1 is a stimulator of IL-6 release from cultured human pituitary adenoma cells that secrete IL-6. Stimulation of IL-6 release by IL-1 in these tumour cells is probably not mediated by prostaglandins or by a pertussis toxin-sensitive mechanism.
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PMID:Interleukin-1 stimulates the release of interleukin-6 from cultured human pituitary adenoma cells. 839 Nov 94


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