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

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

The significance of interleukin-6 (IL-6) in patients with inflammatory bowel disease (IBD) was studied by measuring the IL-6 level in serum and colonic tissue by means of an enzyme-linked immunosorbent assay (ELISA), and by examining its localization using an immunohistochemical method. The serum IL-6 level reflected the degree of disease activity, and the extent of affected area, and was also correlated with the serum C-reactive protein (CRP) level. In the colonic mucosa of active IBD, the tissue IL-6 level was markedly elevated, and immunoreactive products of anti-IL-6 antibody were present in infiltrative mononuclear cells in the lamina propria. This indicates that IL-6 production in these cells is enhanced at the site of affected intestine. These results, together with its biological activity and the type of cell producing it, suggest that IL-6 is an available marker to assess disease conditions of IBD and that it might be also involved in the pathophysiology of IBD.
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PMID:Significance of interleukin-6 in patients with inflammatory bowel disease. 200 57

Metallothioneins are attractive substances. One of the features of these proteins is the inducibility in response to heavy metals, to a great variety of metabolites and to stress factors. In mammalia, their synthesis may be induced by interleukin-6 in response to inflammation. Metallothionein could prevent renal toxicity of cDDP without compromising its anticancer activity. However, metallothionein is also implicated in the resistance to cDDP. There are now good evidences that metallothionein is involved in many diseases, such as inflammatory bowel disease, toxemia of pregnancy, liver disease, etc.
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PMID:[Metallothionein and medicine]. 760 19

Cytokines are important immunoregulatory mediators. Their contribution to the pathogenesis of acute and chronic gastroenterological disorders is obvious. Increased expression of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor (TNF) can be detected in inflammatory bowel disease. During the last few years it has also been recognized that activated leukocytes have an important role in the multisystem involvement of acute pancreatitis. Activation of leukocytes is an early event during severe acute pancreatitis, and it may be a pathogenetic factor in the severity of the disease. The review summarizes the recent findings in the field of inflammatory cytokines with particular attention of TNF, IL-1, IL-6, and IL-8 during severe acute pancreatitis and underscores the role of the activated leukocytes in the pathogenesis of complicated acute pancreatitis.
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PMID:[Inflammatory mediators in acute pancreatitis (theoretical considerations)]. 765 17

Local interleukin-6 (IL-6) activity was studied using colonic mucosal tissues in inflammatory bowel disease (IBD) and inflammatory control patients. Active IBD specimens exhibited significantly higher IL-6 activity than control specimens in both cultures of isolated lamina propria mononuclear cells (LPMC) and mucosal tissues with an increased number of IL-6-producing cells. However, the activity in inactive IBD or inflammatory controls did not differ from controls. Northern blot analysis demonstrated IL-6 messenger RNA in LPMC and colonic epithelial cells isolated from active IBD specimens but not in control cells. Furthermore, immunofluorescent microscopic study of active IBD specimens showed more conspicuous staining of IL-6 in infiltrating LPMC (mostly CD68+ cells) and colonic epithelial cells. These results suggest that elevation of local IL-6 activity may be a characteristic feature of active IBD and both macrophages and colonic epithelial cells are the major cell types responsible for this phenomenon.
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PMID:Elevation of interleukin-6 in inflammatory bowel disease is macrophage- and epithelial cell-dependent. 772 84

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 production of interleukin-6 (IL-6) in patients with inflammatory bowel disease (IBD) has been measured, including the effects of steroid hormone, salicylazosulfapyridine (SASP) and its metabolites. In active Crohn's disease (CD) (n = 12) and ulcerative colitis (UC) (n = 9), rate of IL-6 positive group in serum was significantly higher than that in controls (n = 20) (p < 0.01, p < 0.01). In active CD (n = 9) and UC (n = 9), the level of IL-6 production by peripheral blood mononuclear cells (PBMNC) was 22.8 +/- 15.1 ng/ml, 24.3 +/- 14.4 ng/ml, and it was significantly higher than that in controls (n = 15, 8.0 +/- 6.6 ng/ml) (p < 0.05, p < 0.01). IL-6 production by PBMNC always showed the time dependent increase both in IBD and controls, and the level of IL-6 was always higher in IBD than that in controls during the culture time. Furthermore, IL-6 production by monocyte in UC (n = 6, 4.4 +/- 1.4 ng/ml) was significantly higher than that in controls (n = 6, 1.7 +/- 0.8 ng/ml) (p < 0.01). The effects of steroid hormone, SASP and its metabolites on IL-6 production were also investigated. Steroid hormone significantly reduced IL-6 production by PBMNC, but others had no effect on IL-6 production. This study suggested that IL-6 might be involved in the pathophysiology of IBD.
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PMID:[A study on interleukin-6 in inflammatory bowel disease]. 810 Dec 42


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