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)

Cerebrospinal fluid (CSF) from patients with a variety of central nervous system (CNS) disorders was assayed for cytokines, prostaglandins, and autoantibodies. CSF interleukin-6 (IL-6) in patients with CNS infection (374.24 +/- 92.61 pg/mL) and neuropsychiatric systemic lupus erythematosus (NP-SLE) (71.40 +/- 5.89 pg/mL) were significantly higher than in patients with CNS inflammation (33.92 +/- 29.36 pg/mL) or controls (non-inflammatory CNS diseases) (4.35 +/- 3.00 pg/mL). Interleukin-1 beta, interferon alpha, and tumor necrosis factor alpha were undetectable in these samples: CSF prostaglandin E2 (PGE2) also exhibited similar patterns as IL-6. CSF immunoglobulin G (IgG) in patients with NP-SLE (8.84 +/- 1.80 mg/dL) was much higher than in patients with CNS infection (4.65 +/- 3.09 mg/dL), CNS inflammation (2.54 +/- 1.24 mg/dL), or controls (2.11 +/- 1.03 mg/dL). CSF autoantibodies against calf thymus antigens were present in patients with NP-SLE but not in patients with CNS infection as demonstrated by immunoblot. These results suggest that high IL-6 and PGE2 in CSF favors the diagnosis of CNS infection, while modestly elevated IL-6, high IgG, and autoantibodies against calf thymus antigens in CSF are the features of NP-SLE.
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PMID:Cerebrospinal fluid interleukin-6, prostaglandin E2 and autoantibodies in patients with neuropsychiatric systemic lupus erythematosus and central nervous system infections. 816 38

Cytokines are thought to cause the depression of cytochrome P-450 (CYP)-associated drug metabolism in humans during inflammation and infection. We have examined the role of five cytokines, i.e., interleukin-1 beta, interleukin-4, interleukin-6, tumor necrosis factor-alpha, and interferon-gamma, on the expression of CYP1A2, CYP2C, CYP2E1, CYP3A, and epoxide hydrolase in primary human hepatocyte cultures. Steady state P-450 and epoxide hydrolase mRNA levels, as well as ethoxyresorufin-O-deethylase and nifedipine oxidation activities, which are mainly supported by CYP1A1/1A2 and CYP3A, respectively, were measured. Interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha were found to be the most potent depressors of P-450 enzymes. After 3 days of treatment, both mRNA levels and enzyme activities were depressed, typically by at least 40%, whatever the cytokine and the enzyme considered. Interferon-gamma also suppressed CYP1A2 and CYP2E1 mRNA levels and ethoxyresorufin-O-deethylase activity but had no effect on CYP3A and epoxide hydrolase mRNAs. In addition, interleukin-4 had the opposite effect, compared with other cytokines, on CYP2E1 mRNA, which was increased up to 5-fold; ethoxyresorufin-O-deethylase and nifedipine oxidation activities were not significantly affected. These results provide the first demonstration that various cytokines act directly on human hepatocytes to affect expression of major P-450 genes and that a wide range of responses can be observed among the enzymes for a given cytokine, suggesting that different regulatory mechanisms may be involved.
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PMID:Cytokines down-regulate expression of major cytochrome P-450 enzymes in adult human hepatocytes in primary culture. 823 20

Constitutive and endotoxin (lipopolysaccharide [LPS])-stimulated release of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and prostaglandin E2 (PGE2) by blood monocytes and peritoneal cell preparations from patients on various forms of dialysis was measured. Monocytes were obtained from healthy controls (n = 20), and from patients on peritoneal dialysis (n = 8), on hemodialysis with cellulose ester membranes (n = 9), and on hemodialysis with polysulfone membranes (n = 8). Peritoneal macrophages were recovered by lavage during laparoscopic surgery from 11 healthy controls, from dialysate in 37 patients on peritoneal dialysis, and at catheter placement for transfer to peritoneal dialysis from eight patients on hemodialysis with polysulfone membranes. Peak LPS-induced production of TNF-alpha, IL-1 beta, and IL-6 by monocytes from patients on peritoneal dialysis and cellulose ester hemodialysis was less than that by monocytes from healthy controls. In contrast, monocytes from patients treated with polysulfone hemodialysis produced amounts of cytokine not different from controls. Lipopolysaccharide-stimulated PGE2 production by monocytes was the same in both patient and control groups. Peritoneal cell preparations from patients on peritoneal dialysis showed decreased release of IL-1 beta and TNF-alpha as compared with control peritoneal cells and with their own blood monocytes. To determine whether the decreased response to LPS by peritoneal cells compared with their own blood monocytes could be attributed to lower numbers of macrophages in the peritoneal cell preparations, adherence of peritoneal cells to plastic was performed. Adherence increased the percentage of macrophages from 70% to more than 90%. In monocytes and adherence purified peritoneal macrophages from peritoneal dialysis patients, no significant difference between monocytes and adherent peritoneal macrophages could be found for TNF-alpha and PGE2. Interleukin-1 beta production by the adherent peritoneal macrophages, as by total peritoneal cells, was significantly lower than that by monocytes. Constitutive production of PGE2 and IL-6 by peritoneal cells from patients on peritoneal dialysis was significantly increased. In contrast, LPS-stimulated production of TNF-alpha, IL-1 beta, and IL-6 by blood monocytes and peritoneal cells from patients receiving hemodialysis with polysulfone membranes was comparable to that produced by monocytes and peritoneal cells obtained from healthy controls. Thus, blood monocytes and peritoneal cells from patients on peritoneal dialysis and from patients on hemodialysis with cellulose-ester membranes demonstrate a decreased cytokine response to LPS, suggesting a state similar to endotoxin tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of dialysis modality in responses of blood monocytes and peritoneal macrophages to endotoxin stimulation. 832 72

In this report, we demonstrated that Interleukin-6 (IL-6) production could be induced by stimulating renal cell carcinoma cell lines, namely ACHN, Caki-1 and TC-1 cells with Interleukin-1 beta (IL-1 beta). IL-1 beta had no effects on cell proliferation in ACHN cells. However, IL-1 beta could suppress cell proliferation in Caki-1 and TC-1 cells. Flow cytometric cell cycle analysis by double staining method with propidium iodide and Proliferating cell nuclear antigen (PCNA) disclosed IL-1 beta caused cell accumulation at G1 phase. Fine granules were visualized in perinuclear area of TC-1 cells treated with IL-1 beta under microscopy. High electron density granules and spherically dilated rough endoplasmic reticula were observed by electron microscopic examinations. In TC-1 cell culture, IL-1 beta excretion into the supernatant was demonstrated by bioassay and ELISA. These results suggest that IL-1 beta functions as an "autocrine growth inhibitor" against TC-1 cells. Half-maximal inhibition of IL-1 beta and IFN-alpha was 6.5 pg/ml, and 720 U/ml, respectively for TC-1 proliferation and combination of these cytokines showed enhanced activity in cell growth inhibition.
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PMID:[Demonstration of interleukin-1 (IL-1) as an autocrine growth inhibitor in renal cancer cell line, TC-1]. 841 9

Interleukin-1 beta is a potent mediator of the acute-phase response. However, the effects of interleukin-1 beta administration on the topic in vivo production of acute-phase proteins and albumin are so far not well understood. Overnight fasted rats were subcutaneously injected with 0.2 mL 0.9% NaCl (control group) or 6.25 micrograms recombinant human interleukin-1 beta, and rectal temperature was measured at intervals up to 48 h. Livers were perfused-fixed in vivo prior to injection (base-line), and at 9, 24, and 48 h following the interleukin-1 beta injection. Fibrinogen, orosomucoid (alpha 1-acid glycoprotein) and albumin were immunostained using a streptavidin-biotin-immunoperoxidase technique. Rectal temperature peaked 5 h after the single interleukin-1 beta injection, and fell gradually to base-line values by 24 h. Prior to injection only a few hepatocytes, randomly scattered throughout the liver lobule, stained positive for fibrinogen and orosomucoid. In contrast, all hepatocytes stained uniformly positive for fibrinogen and orosomucoid 9 h after interleukin-1 beta injection, whereas at 24 h a predominant centrilobular staining pattern occurred. Due to fasting, albumin positive hepatocytes were already reduced at base-line in both groups. Interleukin-1 beta induced a further significant loss of albumin positive cells in the periportal zone (35 +/- 21%) at 9 h when compared with controls (58 +/- 11%, p = 0.037). In conclusion, subcutaneous interleukin-1 beta (probably by stimulation of interleukin-6) strongly induces fibrinogen and orosomucoid expression in rat liver, and suppresses immunohistochemically stainable albumin in a heterogenous way, mainly in the periportal zone.
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PMID:Immunohistochemical demonstration of interleukin-1 beta induced changes in acute-phase proteins and albumin in rat liver. 852 85

Frozen sections of 21 gliomas were analysed to characterize inflammatory infiltrating cells, HLA-DR antigen expression and cytokine secretion. Mononuclear cells infiltrating the tumours were mostly macrophages, which were detected in 100% of cases, and expressed HLA-DR antigens. Lymphocytes were less frequently seen and expressed the CD8 phenotype. Interleukin-1 beta (IL-1 beta) and Interleukin-6 (IL-6), two cytokines mainly produced by activated cells of the macrophage lineage, were demonstrated especially in neoplastic astrocytes. IL-1 beta immunoreactivity was detected in all tumours, and was prevalent in more anaplastic gliomas; IL-6 was found in anaplastic gliomas and in glioblastomas. IL-1 receptors were expressed by both infiltrating macrophages and neoplastic astrocytes in the gliomas analysed. These findings suggest that cytokine production in gliomas seems not related to immune reactions against the tumour and their synthesis by anaplastic astrocytes could follow an unregulated activation of many metabolic processes after neoplastic transformation.
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PMID:Immune infiltrates and cytokines in gliomas. 868 25

A variety of cytokines are found in the intestinal mucosa of individuals with inflammatory diseases. The potential role of cytokines in mediating lipoprotein assembly and secretion in the human intestinal cell line, Caco-2, was investigated. Interleukin-1 beta, interleukin-6 (IL-6), and tumor necrosis factor-alpha all decreased the basolateral secretion of apolipoprotein B (apo B), with IL-6 being the most potent. IL-6 was also found to inhibit triacylglycerol secretion. In contrast, transforming growth factor-beta 1 (TGF-beta 1) increased the secretion of apo B and triacylglycerol. In pulse-chase experiments, IL-6 decreased the rate of synthesis and secretion of apo B-100 and apo B-48 without altering the rate of apo B degradation, whereas TGF-beta 1 increased the rate of synthesis and secretion of apo B-100 and apo B-48. Degradation of apo B was also not affected by TGF-beta 1. The abundance of apo B mRNA in cells incubated with IL-6 was decreased, whereas cells incubated with TGF-beta 1 had higher levels of apo B mRNA. In conditions of small intestinal inflammation, cytokines could contribute to the observed malabsorption of fat and other nutrients by the small intestine.
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PMID:Cytokines regulate apolipoprotein B secretion by Caco-2 cells: differential effects of IL-6 and TGF-beta 1. 877 6

Interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), and interleukin-6 (IL-6) were measured in the cerebrospinal fluid (CSF) and plasma of 12 control subjects, 11 sporadic Alzheimer's disease (AD) and 22 de novo Parkinson's disease (PD) patients using high sensitivity enzyme-linked immunosorbent assays (ELISA). IL-1 beta and IL-6 contents were significantly elevated in the CSF of de novo PD and AD patients in comparison to the control group. In contrast, the plasma levels were not significantly affected. IL-2 contents in the CSF and plasma samples were unchanged in the three groups compared. Because the two cytokines IL-1 beta and IL-6 are known to play a key role in the interaction between the nervous and immune system, e.g. in the so-called acute phase response, our results support the involvement of immunological events in the complex process of neurodegeneration in AD and PD.
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PMID:Interleukin-1 beta and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer's and de novo Parkinson's disease patients. 878 20

Interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha and the soluble interleukin-2 receptor were measured in the serum of 34 healthy controls and 48 patients with chronic schizophrenia using ELISA sandwich assays. No differences were found between the controls and patients.
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PMID:Serum cytokine concentrations in patients with schizophrenia. 879 10

The release of monokines such as Tumor Necrosis Factor a (TNF alpha), Interleukin-1 beta (IL-1 beta) and Interleukin-6 (IL-6) by activated monocytes/macrophages is an important step in the immune as well as in the inflammatory response. In this study the production of TNF alpha, IL-1 beta and IL-6 by human monocytes (HM) and peripheral blood mononuclear cells (PBMC) was evaluated after HHV-6 infection. Our results demonstrate that HHV-6 can selectively regulate monokine synthesis, in a time-dependent manner. Moreover, we observed a different response closely related to the cellular population (HM or PBMC) examined. The hypothesis we evaluated was that IFN gamma is an important factor triggering the activation of HHV-6 infected human monocytes, to release monokines.
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PMID:Role of IFN gamma on TNF alpha, IL-1 beta and IL-6 release during HHV-6 infection. 884 Oct 33


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