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)

The etiology of ulcerative colitis (UC) and Crohn's disease (CD) remains enigmatic. Infiltrating intestinal macrophages are capable of producing the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6). We investigated the presence of IL-6, TNF-alpha and IL-1 beta mRNA transcripts in inflammatory bowel disease (IBD), normal, and other inflammatory intestinal specimens utilizing the polymerase chain reaction (PCR). TNF-alpha mRNA levels did not very between inflammatory bowel disease and control specimens. IL-1 beta mRNA levels were highest in active UC and noninflammatory bowel disease inflammatory specimens while IL-6 mRNA levels were highest in active IBD specimens. Infiltrating T cells, macrophages, and B cells were identified as sources of IL-6 protein in inflammatory bowel disease specimens by immunofluorescent staining. IL-6 transcripts were elevated only in active inflammatory bowel disease specimens, suggesting that IL-6-mediated immune processes are ongoing in the inflammatory mucosal environment of CD and UC.
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PMID:Tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 expression in inflammatory bowel disease. 158 85

Inflammatory bowel diseases lead to a systemic acute-phase response. Monocyte activation plays a central role during systemic acute-phase response via secretion of inflammatory cytokines. We determined the activation of peripheral-blood monocytes in patients with inflammatory bowel diseases by measuring their interleukin-6 (IL-6) secretion. Blood was obtained from patients with active Crohn's disease before treatment [mean Crohn's disease activity index (CDAI) = 332 +/- 34] and from patients after treatment with prednisolone (mean CDAI index = 139 +/- 20). The mean serum IL-6 levels measured by a hybridoma growth assay (B9) were 23 +/- 4 U/ml before therapy and fell to 16 +/- 3 U/ml after treatment with prednisolone. Healthy persons and patients with inactive Crohn's disease usually had serum IL-6 levels below the detection limit of 4 U/ml. An ex vivo whole-blood system was used to measure IL-6 secretion by peripheral-blood monocytes with and without stimulation. Spontaneous IL-6 secretion in this system was about 9 U/ml in patients with Crohn's disease and below the detection limit of 4 U/ml in healthy controls. Moderate stimulation of blood cells [100 pg/ml lipopolysaccharide (LPS)] from patients with active Crohn's disease before and after treatment led to mean IL-6 concentrations of 1,160 +/- 514 and 131 +/- 54 U/ml, respectively. Maximal stimulation of peripheral blood before and after therapy by LPS (100 ng/ml) led to mean IL-6 concentrations of 5,570 +/- 1,660 and 6,220 +/- 1,630 U/ml, respectively. Thus, administration of glucocorticoids led to a rapid down-regulation of IL-6 synthesis by peripheral-blood monocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of monocytes during inflammatory bowel disease. 171 13

Peripheral venous plasma concentrations of interleukin-6 were studied in 21 patients with active Crohn's disease, 20 patients with ulcerative colitis, and 16 control subjects. Interleukin-6 was detected in the plasma of 18 of 21 patients with Crohn's disease (median 47 (range less than 20-250) pg/ml) but in only two with ulcerative colitis and two control subjects. In the patients with Crohn's disease there was a significant negative correlation between the plasma interleukin-6 and the serum albumin concentrations. In eight patients with Crohn's disease and five patients with ulcerative colitis undergoing resection plasma from peripheral circulation and mesenteric vein draining diseased intestine was studied. Interleukin-6 was detected in seven of eight peripheral and mesenteric samples from the patients with Crohn's disease but was not detected in any of the samples from the patients with ulcerative colitis. There was no significant difference between mesenteric and peripheral samples in the concentrations of interleukin-6.
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PMID:High circulating concentrations of interleukin-6 in active Crohn's disease but not ulcerative colitis. 177 61

Crohn's disease and ulcerative colitis are chronic inflammatory bowel diseases (IBD) of unknown etiology. They are characterized by an activation of intestinal mononuclear cells. Cytokines play a crucial role in the regulation of the functions of these cells. An increased synthesis of the cytokines interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF alpha), which are primarily synthesized by activated monocytes/macrophages has been described in patients with IBD. The synthesis of interleukin-2 (IL-2) and of interferon gamma (IFN gamma), which are produced by lymphocytes, on the other hand, has been found to be decreased. The published data are, however, not quite consistent. In patients with IBD there is not only a stimulation of the local cytokine production in the gut. The blood levels and the synthesis of the cytokines IL-1, IL-6 and TNF alpha by peripheral blood mononuclear cells are also increased, in particular in patients with Crohn's disease. Drugs, which are commonly used for the treatment of IBD impair the synthesis of these cytokines in monocytes/macrophages.
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PMID:Inflammatory mediators in chronic inflammatory bowel diseases. 179 95

Interleukin-6, a cytokine produced by various cell types, has a major role in inflammatory and immunological reactions. To define its potential role in inflammatory bowel disease, its concentrations in endoscopic biopsy samples from patients with ulcerative colitis and Crohn's disease were measured. The involved colonic mucosa from active disease was found to contain significantly larger amounts of interleukin-6 than that from inactive disease or normal controls. Colonic mucosal interleukin-6 levels correlated well with the grade of macroscopic inflammation, especially in patients with ulcerative colitis. The levels of interleukin-6 decreased in parallel with clinical improvement following the start of therapy in patients with both forms of inflammatory bowel disease. Mucosal interleukin-6 is thus concluded to accurately reflect the degree of colonic inflammation and may be importantly associated with inflammatory and immunological phenomena seen in inflammatory bowel disease.
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PMID:Colonic mucosal interleukin-6 in inflammatory bowel disease. 180 34

Several case reports suggested good effects of interferon-alpha in patients with Crohn's disease. In addition, a decreased production of interferon-alpha in Crohn's disease has been shown in vitro. Treatment with interferon-alpha may activate intestinal natural killer cells and down-regulate the overproduction of inflammatory cytokines like interleukin-6 in Crohn's disease. To evaluate the clinical efficacy of interferon-alpha, we treated 12 patients with a chronic active course of Crohn's disease with recombinant human interferon-alpha prospectively for 24 weeks. Prednisolone was continuously tapered and discontinued at week 12. The end point of the study was the prevention of worsening of clinical symptoms defined with the Crohn's disease activity index and was monitored by acute-phase proteins, interleukin-6 serum concentrations, and endoscopy. The biochemical activity of interferon-alpha was measured by 2',5'-oligo adenylate serum levels. The end point of the study was reached in four patients (33%). In these patients the final Crohn's disease activity index was above 150, which means that they did not achieve clinical remission. All other patients (66%) did not respond to interferon-alpha and had to be withdrawn prematurely. Interferon-alpha did not show any beneficial effect on interleukin-6 or acute-phase protein concentrations and on endoscopic activity. The 2',5'-oligo adenylate levels continuously increased during interferon therapy. Considerable side effects were noted. These results fail to demonstrate a therapeutic role of interferon-alpha in chronic active Crohn's disease.
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PMID:Prospective evaluation of interferon-alpha in treatment of chronic active Crohn's disease. 772 Apr 72

Interleukin-6 (IL-6) has a major function in the regulation of the inflammatory process. We aimed to define its role as a parameter of disease activity and extent in inflammatory bowel disease. Serum concentrations of IL-6 were measured in 28 patients with Crohn's disease (CD) and in 15 with ulcerative colitis (UC) before starting corticosteroid treatment. Disease activity was measured by standard activity indexes. Serum IL-6 levels were increased in patients with CD (36 +/- 8 pg/ml; p < 0.001) and UC (10 +/- 4 pg/ml; p < 0.05) as compared with 25 control patients. A significant correlation between serum IL-6 concentrations and disease activity was found in patients with CD as well as in patients with UC (active CD: 73 +/- 14 pg/ml, inactive disease: < 10 pg/ml, p = 0.003; active UC: 26 +/- 10 pg/ml, inactive disease: < 10 pg/ml, p = 0.004). IL-6 serum levels were related to the acute-phase reactant c-reactive protein (r = 0.51, p < 0.01) in CD patients. The serum IL-6 concentrations were more pronounced in CD of the colon than in disease limited to the small bowel (p < 0.05). In patients with CD as well as in patients with UC, IL-6 serum concentrations showed a higher sensitivity for disease activity (94 and 83%) than serum c-reactive protein levels. In patients without corticosteroid treatment, the IL-6 serum concentration is related to disease activity in CD as well as UC. Serum IL-6 levels show a higher correlation with disease activity than c-reactive protein levels.
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PMID:Serum interleukin-6 is related to disease activity but not disease specificity in inflammatory bowel disease. 776 91

Etiology and pathogenesis of inflammatory bowel disease (IBD) remain obscure. There is substantial evidence that proinflammatory cytokines such as Interleukin-1 beta (IL-1 beta), Interleukin-6 (IL-6) and Tumour Necrosis Factor-alpha (TNF-alpha) exhibit a key role in the the inflammatory process. In situ hybridisation can depict individual cells producing cytokine mRNA. We performed hybridisation with antisense probes specific for IL-1 beta, IL-6 and TNF-alpha on sections of paraffine-embedded biopsies. Specimens obtained from three control persons and six cases of Crohn's disease (CD) were investigated. Only few positive cells were found in tissue sections of control persons, clusters of lamina propria cells or epithelial cells containing cytokine mRNA were not observed. Inflammatory bowel disease tissue contained large numbers of cells producing mRNA specific for the three proinflammatory cytokines assayed. IL-1 beta, IL-6 and TNF-alpha mRNA were predominantly detected corresponding to cells of the lamina propria. Single cells containing mRNA specific for IL-6 were also found among the epithelial lining of intestinal crypts. Epithelial cells containing IL-1 beta and IL-6 mRNA were found in specimens derived from one patient with Crohn's disease. Notably, large amounts of cells containing cytokine mRNA were not only found in inflamed, but also in macroscopically normal mucosa. In conclusion, using proinflammatory cytokines as a model, we established in situ hybridisation on sections of mucosal biopsies permitting further insight into immune activation at individual cell level.
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PMID:Cytokine expression in intestinal mucosal biopsies. In situ hybridisation of the mRNA for interleukin-1 beta, interleukin-6 and tumour necrosis factor-alpha in inflammatory bowel disease. 784 54

The authors summarize the recent findings obtained in the field of inflammatory cytokines with particular attention on interleukin-6 (IL-6). After a short review of the molecular biology and of the cellular effects of IL-6, the most important clinical relations of IL-6 in hepatic diseases, in non-specific inflammatory bowel diseases (Crohn's disease and ulcerative colitis) and in certain autoimmune diseases are provided. The simultaneous discussion of molecular and clinical data contribute to the understanding of pathomechanisms.
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PMID:[Interleukin-6: friend or enemy? Latest findings on the clinical aspects of IL-6]. 770 Jun 21

Intestinal blood loss as well as chronic inflammation are regarded as the most important mechanisms in the pathogenesis of anemia in Crohn's disease. In addition, cytokines such as interleukin-6 can suppress erythropoietin production. This study was performed to investigate the importance of iron status, inflammatory activity, and endogenous erythropoietin concentrations for the development of anemia in Crohn's disease. In 49 consecutive patients with Crohn's disease, hemoglobin, inflammatory activity (Crohn's disease activity index, C-reactive protein, alpha 1-acid glycoprotein), iron status (serum iron, transferrin, transferrin saturation, ferritin), and serum erythropoietin levels were studied. Anemic (Hb < 12.0 g/dl; N = 16) vs nonanemic patients (Hb > or = 12 g/dl; N = 33) showed reduced iron compartments (eg, ferritin 28.7 +/- 12.9 micrograms/liter vs 63.2 +/- 15.0 micrograms/liter, transferrin saturation 6.2 +/- 1.4% vs 11.5 +/- 1.3%, P < 0.01) but no differences in inflammatory activity. An inverse correlation between erythropoietin and hemoglobin concentrations was found (r = -0.62; P < 0.001), but the increase in erythropoietin levels was inadequate to the degree of anemia. There was no correlation between erythropoietin and interleukin-6 serum levels. Four of five anemic patients with hemoglobin below 10.5 g/dl and erythropoietin levels within the normal range were treated with parenteral iron (200 mg iron saccharate in 250 ml NaCl, weekly, intravenously). Two of them additionally received recombinant human erythropoietin (150 units/kg, 3x weekly, subcutaneously). After five weeks all patients had a marked increase in hemoglobin. However, the mean increase in erythropoietin-treated patients was 5.0 g/dl compared to 2.0 g/dl in the patients with iron therapy only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anemia in Crohn's disease. Importance of inadequate erythropoietin production and iron deficiency. 808 99


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