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 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

To investigate the relationship between serum concentrations of interleukin-8 (IL-8) and disease activity in inflammatory bowel disease, serum IL-8 concentrations were measured by enzyme-linked immunosorbent assay (ELISA) in 93 patients. Interleukin-8 levels were compared with plasma interleukin-6 (IL-6) levels in 80 of these patients. Interleukin-8 levels were also measured in ten patients with active Crohn's disease, before and after treatment with a defined formula polymeric diet. Of these patients, 70 out of 93 IL-8 concentrations were below the detection limit of the assay. Levels were higher in patients with active ulcerative colitis (median < 20 pg/mL, 75th centile value = 190) compared with inactive disease (median and 75th centile value < 20; P < 0.05). Interleukin-8 concentrations correlated with a combined score for disease severity and extent (P = 0.01). Thirty-eight per cent (8/20) of patients with active Crohn's disease also had high levels of IL-8 but there was no significant difference between active and inactive disease. There was no correlation between serum IL-8 and plasma IL-6; on the contrary, very few patients had raised blood levels of both cytokines. In the diet treated group, serum IL-8 fell significantly after treatment (median = 37 pg/mL, range < 20-4615 before treatment, median < 20, range < 20-104 after treatment; P = 0.03). The results suggest that although IL-8 may be involved in the inflammatory process in inflammatory bowel disease, it is a poor marker of disease activity.
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PMID:Serum interleukin-8 in inflammatory bowel disease. 828 Aug 36

Acute phase proteins are released from the liver in response to cytokines, and measurement of serum concentrations offers a valuable means of assessing inflammatory bowel disease. C-reactive protein (CRP) is a participating prominent component of the acute phase response in active Crohn's disease. This study aimed at determining the comparative role of the cytokines interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6), in driving CRP production in inflammatory bowel disease, and to test the hypothesis that there is a difference in the profile of cytokines generated in these two conditions. Serum CRP, the release of the cytokines IL-1 beta and IL-6 from monocytes, and the ability of monocyte conditioned medium to stimulate CRP synthesis by hepatocytes in an in vitro system was measured in patients with ulcerative colitis and Crohn's disease. Monocytes from patients with Crohn's disease produced more 1L beta-1 than monocytes from patients with ulcerative colitis or normal controls. There was no increased tendency for monocytes from Crohn's disease patients to produce more 1L-6, so the greater circulating values of IL-6 reported by a number of authors in Crohn's disease may reflect the participation of a larger number of cells of the monocyte-macrophage series, or production of IL-6 by other cell types. Correlation of cytokine production by monocytes with in vitro CRP release from cultured hepatocytes in response to monocyte conditioned medium showed that, in that system, IL-1 beta was the stronger stimulus to CRP production. Some of the differences in the inflammatory processes of ulcerative colitis and Crohn's disease may reflect differences in the amount of IL-1beta and IL-6 generated from macrophages and monocytes.
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PMID:Interrelations between interleukin-6, interleukin-1 beta, plasma C-reactive protein values, and in vitro C-reactive protein generation in patients with inflammatory bowel disease. 820 May 75

Using metabolic labeling techniques in human intestinal epithelial cell lines in tissue culture and in situ hybridization techniques in normal and inflamed (Crohn's) intestine, recent studies have shown that there is synthesis of acute phase proteins in enterocytes. Moreover, these studies have shown that acute phase protein biosynthesis in enterocytes is regulated by inflammatory cytokines in a manner characteristic of the physiologic acute phase response. In the course of these studies it was noticed that one inflammatory cytokine, interleukin-6 (IL-6), mediated selective down-regulation of the enterocyte-specific, differentiation-dependent integral membrane protein sucrase-isomaltase (SI) in the Caco2 intestinal epithelial cell line. In the current study we examined the effect of several other inflammatory cytokines interleukin-1 (IL-1 beta), tumor necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma) on synthesis of SI in Caco2 cells, examined the possibility that inflammatory cytokines affect the synthesis of other enterocyte integral membrane proteins using lactase as a prototype, and examined the possibility that SI gene expression was down-regulated in villous enterocytes in vivo during the local inflammatory response of Crohn's disease. The results show that IL-6 and IFN gamma each mediate a decrease and TNF alpha mediates an increase in synthesis of SI in Caco2 cells. The magnitude of down-regulation by IL-6 and IFN gamma is significantly greater than the up-regulation by TNF alpha. IL-1 beta has no effect on synthesis of SI. Synthesis of lactase is not affected by any of the cytokines. There is a marked specific decrease in SI gene expression in villous enterocytes in acutely inflamed Crohn's ileum as compared to adjacent uninflamed ileum and normal ileum. Taken together, these data show that inflammatory cytokines have specific and selective effects on the expression of the brush border hydrolase SI in tissue culture and in vivo and provide evidence for a previously unrecognized mechanism for disaccharidase deficiency in intestinal inflammation.
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PMID:Regulation of sucrase-isomaltase gene expression in human intestinal epithelial cells by inflammatory cytokines. 855 56

Chronic inflammation in inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) may be attributed partly to increased secretion of inflammatory cytokines. The aim of this study was to investigate simultaneously the spontaneous release patterns of tumor necrosis factor-alpha (TNF-alpha), interleukin-1-beta (IL-1 beta), and interleukin-6 (IL-6) by organ cultures of inflamed mucosa from IBD patients. Organ cultures of involved IBD mucosa spontaneously produced increased amounts of TNF-alpha, IL-1 beta, and IL-6 compared to normal mucosa. The patterns of cytokine release between Crohn's disease and ulcerative colitis organ cultures were not significantly different. Increased inflammatory cytokine production by lamina propria mononuclear cells (LPMCs) and mucosa treated with EDTA suggests that these cytokines originate mainly from LPMCs. These results confirm the role of inflammatory cytokines in IBD and shed a new light on the role of TNF-alpha in IBD.
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PMID:Mucosal inflammatory cytokine production by intestinal biopsies in patients with ulcerative colitis and Crohn's disease. 873 57

Previous studies have demonstrated elevated serum levels of interleukin-6 (IL-6) and the soluble interleukin-2 receptor (IL-2R, CD25) in individuals with inflammatory bowel disease (IBD). The aim of our study was to compare serum IL-6 and IL-2R levels to see if one marker better distinguished IBD from other intestinal disorders or better reflected disease activity. Blood samples were obtained from 41 pediatric patients with Crohn's disease, 22 with ulcerative colitis, 19 with other gastrointestinal inflammatory disorders, and 13 with functional abdominal pain. Disease activity and disease location were determined for patients with Crohn's disease and ulcerative colitis. Serum levels of IL-6 and IL-2R were determined by using an enzyme-linked immunosorbent assay. Mean serum levels of IL-6 were significantly elevated (p < 0.05) in patients with Crohn's disease when compared with individuals with ulcerative colitis, other gastrointestinal inflammatory disorders, or functional abdominal pain. By comparison, there was no significant difference in mean serum levels of IL-2R in individuals with Crohn's disease compared with these other groups. Patients with moderate/severe Crohn's disease had elevated mean serum levels of IL-6 and IL-2R when compared with those with mild and inactive disease (p < 0.05); however, neither marker distinguished between inactive and mild disease. IL-6 correlated better with the erythrocyte sedimentation rate (ESR; r = 0.57, p < 0.001) than did IL-2R (r = 0.28, p < 0.01). Our results suggest that elevated IL-6 levels a.e more likely to be seen in patients with Crohn's disease. Although IL-6 may be a better marker for Crohn's disease and active disease than IL-2R, it does not appear to offer any advantage over the ESR.
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PMID:Elevation of serum interleukin-6 but not serum-soluble interleukin-2 receptor in children with Crohn's disease. 885 84

Many attempts have been made over recent years to assess accurately disease activity in Crohn's disease. We review some of these attempts, giving particular emphasis to the combination of serum levels of proinflammatory cytokines (interleukin-6, tumour necrosis factor alpha, recombinant interleukin-2 and acid alpha-1-glycoprotein).
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PMID:Assessing disease activity in Crohn's disease--are we there yet? 939 81

Interleukin-10 is an important cytokine that is involved in regulation of pro-inflammatory cytokines and T-cell responses. Interleukin-10 has been studied extensively in various preclinical and clinical models of inflammation. The most remarkable and consistently reproducible quality of IL-10 is its ability to downregulate macrophage functions. This includes inhibiting the production of pro-inflammatory cytokines such TNF-alpha, Interleukin-1, Interleukin-6 and antigen presentation by these professional antigen presenting cells. Additionally, Interleukin-10 also has effects on various other cell types of hematopoietic origin such as B-cells, neutrophils, and most importantly T-cells. Interleukin-10 has shown efficacy in several models of autoimmune disease. The present article deals with the effect of Interleukin-10 in animal models of inflammatory bowel disease and the results of phase I clinical trials in normal human volunteers and chronic active Crohn's disease patients.
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PMID:Immunomodulation of Crohn's disease by interleukin-10. 942 29

Many nutritional issues are important in the care of children and adolescents with inflammatory bowel disease. No specific dietary toxin or antigen has been identified to have an etiologic role in either ulcerative colitis or Crohn's disease. A possible modulating effect of omega-3 polyunsaturated fatty acids on intestinal inflammation is being investigated. Most prevalent among the nutritional consequences of inflammatory bowel disease is weight loss, for which inadequate caloric intake is primarily responsible. Impairment of linear growth and associated delay in pubertal development commonly complicate childhood Crohn's disease. The two major etiologic factors are chronic undernutrition and direct effects of inflammatory mediators secreted from the inflamed gut. Recent studies have incriminated interleukin-6. Treatment of intestinal inflammation and provision of adequate nutrition are of paramount importance in preventing or remedying growth impairment. Exclusive enteral nutrition using formulated food is efficacious primary therapy of active Crohn's disease, although the mode of action is poorly understood.
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PMID:Inflammatory bowel disease. 978 63

Interleukin-6 is one of the most well-characterized cytokines with pleiotropic properties. Besides its B-lymphocyte activation role in hematopoiesis, interleukin-6 plays a central role in regulation of systemic inflammation. Interleukin-6 binds to receptors on target cells (such as hepatocytes and lymphocytes), consisting of an 80 kDa binding chain and gp130, a polypeptide responsible for signal transduction. In addition to the detection of elevated amounts of interleukin-6 in the blood, gene expression (mRNA) of subunits of the interleukin-6 receptor complex have also been studied by examining the reverse transcriptase polymerase chain reaction on peripheral lymphocytes from patients with characteristic radiological symptoms suffering from Crohn's disease. Our data show significantly elevated gene expression both of the 80 kDa interleukin-6 binding chain and gp130. These results suggest that enhancement of the expression of the constituents of interleukin-6 and the interleukin-6 receptor system plays a relevant role in systemic inflammation in inflammatory bowel disease.
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PMID:Increased interleukin-6 levels, interleukin-6 receptor and gp130 expression in peripheral lymphocytes of patients with inflammatory bowel disease. 986 12


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