Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The production of cytokines in peripheral blood mononuclear leukocytes of patients with inflammatory bowel disease was investigated. T cell subset analysis and differential white blood cell counts were also performed. Thirty five patients with ulcerative colitis, 14 with Crohn's disease, and 15 age matched healthy volunteers were studied. No differences were observed in T cell subsets and OKT4/OKT8 ratios in patients with ulcerative colitis or Crohn's disease compared with controls. Interleukin 1 beta production was significantly increased in active ulcerative colitis and Crohn's disease, compared with values in controls, but returned to control levels in the inactive stages. In addition, in active ulcerative colitis and Crohn's disease, there were significant correlations between the interleukin 1 beta production and the ulcerative colitis activity index or Crohn's disease activity index. Interleukin 2 production was also significantly increased in the active ulcerative colitis and significantly correlated to the activity index, but there was no change in Crohn's disease patients compared with controls. Gamma interferon production in patients was the same as that in controls. This study suggests that the interleukin 1 beta and 2 values in peripheral mononuclear leukocytes of active untreated inflammatory bowel disease are indicators of the disease states of ulcerative colitis or Crohn's disease, or both.
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PMID:Cytokine production in patients with inflammatory bowel disease. 164 32

Elevated constitutive expression of major histocompatibility (MHC) class II antigens occurs in the enterocytes of patients with IBD. It has been suggested that this aberrant expression of class II molecules may play a role in the pathogenesis of IBD. We examined two possible reasons for such a finding. 1) Heightened sensitivity of IBD enterocytes to endogenous gamma interferon (gamma IFN) and 2) enhanced endogenous secretion of gamma interferon by intestinal cells in close proximity to the enterocytes (lamina propria lymphocytes). Constitutive and gamma interferon stimulated HLA-DR and DP density on intestinal epithelial cells (IEC) and peripheral blood monocytes (PBM) from UC patients (IEC n = 13; PBM n = 20), CD patients (IEC n = 14; PBM n = 18) and non-IBD controls (IEC n = 12; PBM n = 20) were measured via flow cytometry (mean channel fluorescence). gamma IFN production by PHA stimulated and unstimulated lamina propria lymphocyte (LPL) cultures of UC patients (n = 11) CD patients (n = 8) and non-IBD controls (n = 11) was measured using a vesicular stomatitis virus/WISH cell bioassay. We found significantly greater gamma IFN secretion by IBD-derived PHA stimulated LPL than from non-IBD stimulated controls (CD = 39.4 +/- 12.4u; UC41.5 +/- 6.8u; NL = 22.4 +/- 8.3u, p less than 0.05) while gamma IFN induced HLA-DR and DP upregulation was no greater in IBD-derived IEC and PBM than in non-IBD controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The expression and regulation of class II antigens in normal and inflammatory bowel disease peripheral blood monocytes and intestinal epithelium. 193 20

The activity of an interferon induced enzyme, (2',5') oligo adenylate synthetase, was determined in peripheral blood mononuclear cells and granulocytes of patients with inflammatory bowel disease and compared with its activity in cells isolated from normal subjects. In spite of the fact that circulating interferon is detected in patients with inflammatory bowel disease, we failed to see any increase in (2',5') oligo adenylate synthetase activity in these patients. The mean +/- SE enzyme activity given in nmol ATP incorporated into (2',5') isoadenylate oligomers by extracts of 10(5) peripheral blood mononuclear cells/21 hours was in normal subjects 1.84 +/- 0.30 (n = 27), in patients with active Crohn's disease 1.38 +/- 0.15 (n = 20) and in patients with active ulcerative colitis 1.14 +/- 0.23 (n = 21). (2',5') oligo adenylate synthetase activity in granulocytes was also similar in normal subjects and in patients with active ulcerative colitis or Crohn's disease. The enzyme activity in patients with active disease was similar both prior to and during steroid therapy. The low (2',5') oligo adenylate synthetase activity in peripheral blood mononuclear cells and granulocytes of patients with active inflammatory bowel disease may reflect decreased cellular response to interferon or a difference in the type of interferon elevated in viral diseases and in inflammatory bowel disease.
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PMID:(2'-5') oligo adenylate synthetase activity in leucocytes of patients with inflammatory bowel disease. 240 70

The effect of interferon (IFN) on prostaglandin E2 (PGE2) synthesis by peripheral blood mononuclear cells of normal subjects and patients with inflammatory bowel disease was studied. Exposure of peripheral blood mononuclear cells, isolated from normal subjects and patients with active ulcerative colitis and Crohn's disease, to IFN reduced the release of PGE2 in a dose-dependent manner. The inhibitory effect was observed for at least 24 h after the removal of IFN. To correlate the effect of IFN on PGE2 synthesis with a known activity of IFN, the induction of (2'-5')oligoadenylate synthetase (OAS) was also studied in the same mononuclear cells. Low basal levels of this enzyme were detected in mononuclear cells isolated from normal subjects and patients with active ulcerative colitis and Crohn's disease. Moreover, IFN treatment in vitro resulted in a similar induction of this enzyme in patients and controls. There results indicate that peripheral blood mononuclear cells of patients with active ulcerative colitis and Crohn's disease have normal response to IFN. In addition, our data do not suggest that IFN has an important role in the pathogenesis of these diseases.
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PMID:Interferon inhibits prostaglandin E2 synthesis and stimulates (2'-5')oligoadenylate synthetase activity in peripheral blood mononuclear cells of inflammatory bowel disease patients. 241 32

In a previous study using total mononuclear cells and lymphocytes, enriched by elutriation centrifugation, of patients with Crohn's disease and ulcerative colitis were found to have a decreased NK cell activity. In the present study the relation with disease activity and treatment, and the effect of recombinant gamma-interferon (gamma-IFN) on NK cell and monocyte cytotoxicity has been studied in 19 patients with Crohn's disease, 11 with ulcerative colitis, two with indeterminate colitis and 12 healthy controls. Patients with active Crohn's disease and active ulcerative colitis were shown to have an impaired NK cell activity compared to the control group. However, no difference was found in the percentage of CD16 (Leu 11+) cells, as determined by fluorocytometry, between patients with active or inactive disease. Moreover, the NK cell impairment was not related to corticosteroid treatment. Recombinant gamma-interferon (gamma-IFN) stimulated significantly the cytotoxic activity of the total mononuclear cells and the monocyte-enriched fraction against all target cell lines, both in patients and controls. No relation was found between the increase in cytotoxicity by gamma-IFN and disease activity in the patients. Stimulation with gamma-IFN demonstrated that the monocyte cytotoxic response of inflammatory bowel disease patients is normal. The present study reveals that the impairment in NK cell activity in patients with inflammatory bowel disease is related to disease activity and therefore suggests to be secondary to the inflammatory process.
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PMID:In vitro cellular cytotoxicity in Crohn's disease and ulcerative colitis: relation with disease activity and treatment, and the effect of recombinant gamma-interferon. 251 28

Serum interferon (IFN) of alpha-class was studied in 64 consecutive patients, 26 with Crohn's disease, 38 with ulcerative colitis, and in 34 healthy volunteers. Detectable IFN-alpha in 10 patients was associated with a moderate to severe activity of chronic inflammatory bowel disease (CIBD). However, 19 of 28 patients (68%) with activity in their disease did not have elevated IFN-alpha levels. The three groups, ulcerative colitis, Crohn's disease, and healthy volunteers did not reveal any statistically significant difference in serum IFN-alpha, as four of 34 healthy controls without intercurrent infections had elevated levels as well. Possible effects of alpha, beta, and gamma classes of IFN on endogenous arachidonic acid (AA) release and metabolism in human neutrophils was investigated in a substudy. IFN-alpha caused a dose-dependent release of AA from phospholipids and metabolism of a modest fraction of leukotriene B4 (LTB4) and 5-hydroxyeicosatetraenoic acid (5-HETE) at doses reaching a maximum of 100 IU/ml. IFN of the beta and gamma classes did not exert such effects. Addition of complement 5a to cells activated by IFN-alpha caused induction of increased 5-lipoxygenase activity with unchanged release of AA. As only 16% of all CIBD patients had elevated IFN-alpha levels as compared to 12% among the group of healthy volunteers, IFN-alpha does not seem to be of importance for the perpetuation of the inflammatory reaction in ulcerative colitis or Crohn's disease, and other factors may therefore be responsible for activation of the inflammatory cells to production of LTB4 and 5-HETE.
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PMID:Serum interferon activity in inflammatory bowel disease. Arachidonic acid release and lipoxygenation activated by alpha-class interferon in human neutrophils. 283 22

Gamma interferon (IFN-gamma) production by peripheral blood mononuclear cells (PBM) was measured in 21 patients with Crohn's disease, in 15 patients with ulcerative colitis, in 12 patients with non-IBD gastrointestinal disease (disease control), and in 28 healthy controls. T-cell subset proportions and serum levels of thymosin alpha 1 and thymosin beta 4, two hormonelike thymic peptides, were also determined. No differences were seen in T-cell subset proportions in patients with Crohn's disease or ulcerative colitis when compared to healthy controls or to the disease-control group. In vitro IFN-gamma production was markedly decreased in Crohn's disease and in untreated, but not treated, patients with ulcerative colitis. Preincubation of PBM prior to the addition of inducer mitogen resulted in enhanced IFN-gamma production in patients with Crohn's disease or ulcerative colitis which significantly exceeded that seen either in healthy controls or in the disease-control group. Serum thymosin alpha 1 levels were comparable in all study groups; however, serum thymosin beta 4 concentrations were significantly higher in all patient groups than in the healthy controls. These results confirm a defective in vitro IFN-gamma production in patients with IBD which is apparently independent of endocrine thymus regulation.
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PMID:Defective in vitro gamma interferon production and elevated serum immunoreactive thymosin beta 4 levels in patients with inflammatory bowel disease. 312 96

Immune (gamma) interferon is a substance produced by immunologically activated mononuclear cells. Besides its antiviral activity, interferon gamma has a crucial role in immunoregulation, by acting directly upon lymphocytes and monocytes, and interacting with other soluble mediators of the immune response. Studies of the interferons system in inflammatory bowel disease have been limited, and little information is available on the generation of interferon during immunological events occurring in the human gut. To investigate the capacity of intestinal mucosal mononuclear cells to produce interferon gamma, lamina proprial mononuclear cells, isolated from Crohn's disease, ulcerative colitis, and control patients, were incubated with interleukin 2 or phytohemagglutinin, and the amounts of interferon gamma present in the culture supernatants were measured by a virus cytopathic effect inhibition assay. Under identical stimulatory conditions, culture supernatants of cells derived from actively involved mucosa of inflammatory bowel disease specimens contained two- to fivefold less interferon gamma than those of cells from control tissue. However, the amount of interferon gamma present in supernatants of cells from uninvolved inflammatory bowel disease mucosa was similar to that found in control supernatants. These results indicate that, in patients with active Crohn's disease and ulcerative colitis, mononuclear cells produce decreased amounts of interferon gamma in the intestinal mucosa. The exact significance of these findings is unclear, but because of the importance of interferon gamma in a variety of cell-mediated immune phenomena, its impaired availability might be relevant to the pathogenesis of inflammatory bowel disease.
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PMID:Interferon gamma production by human intestinal mucosal mononuclear cells. Decreased levels in inflammatory bowel disease. 313 80

Colonic epithelial cells (CEC) were isolated from actively inflamed mucosa of IBD patients and checked for HLA-DR, HLA-DP, and HLA-DQ. Half of the freshly isolated CEC from IBD tissue expressed DR, and one third were positive for DP and DQ. Normal human CEC were then cultured for 24 h and their expression of these markers in response to different types of in vitro stimulation was investigated. A significant increase in the expression of DR, DP and DQ was observed in response to the nonspecific mitogen phytohaemagglutinin (PHA), the lymphokine gamma-interferon (gamma-IFN) and the epidermal growth factor (EGF). The enhancement of DR expression was more marked than that of DP and DQ. The effect of gamma-IFN was more rapid and significantly more marked than that of either PHA and EGF for all three antigens. EGF appeared to be more potent than PHA in enhancing the expression of DP and DQ. The data from this study indicate that HLA-D region antigens can be induced on human CEC by different types of stimuli and provide further evidence that the expression of these markers in the colonic epithelium is a normal event the magnitude of which can increase under various circumstances. The data also suggest that the increased expression of HLA-D region antigens by IBD CEC occurs as a result of different mechanisms, and that this expression is an indicator of the active participation of the colonic epithelium to the mucosal inflammatory response.
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PMID:HLA-D region antigens on isolated human colonic epithelial cells: enhanced expression in inflammatory bowel disease and in vitro induction by different stimuli. 314 53

The activity of (2'-5')oligoadenylate synthetase, an enzyme induced by and mediating the antiviral action of interferon, was measured in extracts of intestinal mononuclear and epithelial cells isolated from patients with Crohn's disease, ulcerative colitis, and a control group. No significant differences were detected among (2'-5')oligoadenylate synthetase activities of lamina propria mononuclear cells derived from inflammatory bowel disease-involved and histologically normal control mucosa. Similarly, epithelial cells from inflammatory bowel disease and control patients expressed comparable levels of the enzyme, but these were significantly higher (p less than 0.01) than those found in autologous mononuclear cells. These results indicate that interferon is locally produced along the human intestinal mucosa under normal and inflammatory conditions. While this study supports the contention that induction of an antiviral state does not play a significant role in the pathogenesis of inflammatory bowel disease, it does not exclude the activation of the interferon system for other immunologic functions.
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PMID:(2'-5')Oligoadenylate synthetase activity in intestinal mononuclear and epithelial cells of inflammatory bowel disease patients. 320 Nov 31


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