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 risk of colorectal carcinoma is increased among patients with longstanding ulcerative colitis and Crohn's disease. The development of cancer in inflammatory bowel disease is hypothesized to evolve by a multistep process involving genetic instability, clonal expansion and the development of a malignant phenotype. The contribution of nutritional factors such as folate deficiency is of great interest; molecular genetic mechanisms are under study. In contrast to sporadic colorectal carcinoma, carcinomas in ulcerative colitis are associated with a long prior history of chronic inflammation and the subsequent development of epithelial dysplasia. Dysplasia is defined as an unequivocal neoplastic alteration of the colonic mucosa. The object of surveillance is prevention of death from cancer by detection at a premalignant or early curable stage. Patients at greatest risk of cancer who customarily undergo endoscopic surveillance are those with extensive colitis of more than 8 years duration. Dysplastic epithelium may occur in flat mucosa, and may produce a plaque or a nodular/villiform appearance. Dysplasia is not present in all patients with cancer in colitis. It is important to develop more sensitive and specific markers for the presence of precancer or cancer in colitis. Under study are proliferation-associated markers detected by immunohistochemistry, lectin binding, flow cytometry and laser-induced fluorescence coupled with endoscopy.
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PMID:Ulcerative colitis and colon cancer: biology and surveillance. 146 4

Epithelial histocompatibility locus antigen (HLA) class II expression was studied to evaluate its induction by mucosal mononuclear cells in inflammatory bowel disease and to characterise the responsible cytokine. Unstimulated cells of the HT-29 epithelial cell line did not produce class II molecules. After being stimulated with the mitogenic lectin phytohaemagglutinin mucosal mononuclear cells released a cytokine that induced epithelial HLA-DR expression. The cytokine had the physicochemical and immunological characteristics of interferon-gamma, and no additional cytokines were detected.
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PMID:Characterisation and quantification of mucosal cytokine that induces epithelial histocompatibility locus antigen-DR expression in inflammatory bowel disease. 156 49

Previous reports of a selective mucin subclass defect in ulcerative colitis have been reassessed using high performance chromatography (Superose 6 and Mono Q) for mucin purification and fractionation coupled with analysis of the fractions obtained using a combination of enzyme linked lectin and mucin antibody assays. Mucin samples purified from snap frozen rectal biopsy specimens obtained from patients with ulcerative colitis (n = 12), Crohn's disease (n = 5), and non-inflammatory bowel disease control subjects (n = 9) were subject to ion exchange chromatography using a continuous 0-0.35 mol/l NaCl salt gradient with a final 2.5 mol/l NaCl step. In all samples the major proportion (mean (SD) 86.7 (8.9)%) of the mucin detectable by wheat germ agglutinin binding eluted between 0.15 and 0.35 mol/l NaCl with no significant difference in elution profile between ulcerative colitis and control subjects. Significant elution of glycoprotein at less than 0.15 mol/l NaCl did occur, however, when a lower molecular weight mucin containing fraction which contained concanavalin A positive (glucose or mannose containing) material was analysed similarly. Similar ion exchange profiles were obtained when (3H)N-acetylglucosamine labelled mucins were studied after tissue culture of rectal biopsy specimens. No significant alteration in the ion exchange profile of purified mucins in ulcerative colitis has been shown in these studies. It is possible that the previously reported relative depletion of mucin subclass IV (eluting with 0.20 mol/l NaCl) may simply have reflected mucin depletion.
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PMID:Ion exchange chromatography of purified colonic mucus glycoproteins in inflammatory bowel disease: absence of a selective subclass defect. 195 68

Ulceration anywhere in the gastrointestinal tract induces a novel cell lineage, which grows from the bases of existing crypts, ramifies to form a new gland, and ultimately emerges onto the mucosal surface. The lineage produces neutral mucin, shows a unique lectin-binding profile and immunophenotype, and secretes abundant immunoreactive epidermal growth factor/urogastrone (EGF/URO). All gastrointestinal stem cells can produce this cell lineage following mucosal ulceration, secreting EGF/URO to stimulate cell proliferation, regeneration and ulcer healing. This cell lineage is very commonly associated with gastrointestinal ulceration, and we propose that a major in vivo role for EGF/URO is to stimulate ulcer healing throughout the gut via induction of this cell lineage in the adjacent mucosa. EGF/URO should therefore be assessed in the conservative management of inflammatory bowel disease.
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PMID:Ulceration induces a novel epidermal growth factor-secreting cell lineage in human gastrointestinal mucosa. 226 47

We investigated the ability of isolated human colonic epithelial cells to express the common acute lymphoblastic leukemia antigen (CALLA), the transferrin receptor, and the 4F2 antigen in response to different types of stimuli. The expression of these markers was assessed by immunofluorescence using monoclonal antibodies. Thirty-two percent of freshly isolated colonic epithelial cells from actively inflamed mucosa of patients with inflammatory bowel disease expressed the 4F2 antigen, 28% the transferrin receptor, and 13% the CALLA. Normal colonic epithelial cells were cultured and the kinetics of expression of the three antigens was studied. A significant increase in the expression of the three markers was observed throughout the culture period in response to the lectin phytohemagglutinin and the epidermal growth factor. The kinetics of expression of the 4F2 antigen and the CALLA after lectin stimulation appeared to differ from that observed after epidermal growth factor. At the end of the cultures one-third of the cells expressed the 4F2 antigen and the transferrin receptor, whereas one-fifth were positive for CALLA. Thus, after these cultures the expression of the three markers was quantitatively similar to that observed with freshly isolated cells from inflamed mucosa. gamma-Interferon markedly induced the 4F2 antigen but had no effect on the transferrin receptor and the CALLA. These data demonstrate that colonic epithelium is capable of expressing the 4F2 antigen and the CALLA in association with the transferrin receptor.
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PMID:Ability of human colonic epithelium to express the 4F2 antigen, the common acute lymphoblastic leukemia antigen, and the transferrin receptor. Studies in inflammatory bowel disease and after in vitro exposure to different stimuli. 253 Nov

Previous studies have shown that sera from patients with pancreatic cancer often contain a mucus glycoprotein that expresses the oncofetal antigen galactose 1-3, N-acetyl galactosamine, which is the T blood group antigen and the binding site for the lectin peanut agglutinin (PNA). An enzyme-linked lectin assay has been developed to quantify PNA-binding glycoproteins in serum and has been evaluated as a serological test for pancreatic cancer. Sera were studied from 53 patients with pancreatic cancer and 154 controls, including benign obstructive jaundice, acute and chronic pancreatitis, chronic liver disease and inflammatory bowel disease. The enzyme-linked peanut lectin assay proved highly reproducible and has 77% sensitivity and 83% specificity for pancreatic cancer, results that are very similar to those achieved in the same sera by CA19-9 radioimmunoassay (75% sensitivity, 82% specificity with the upper limit of normal set at 37 u ml-1). CEA assay proved less useful (60% sensitivity, 47% specificity). In this study better results were obtained if an upper limit of normal of 50 u ml-1 was used for CA19-9 (75% sensitivity, 92% specificity). Combination of CA19-9 assay with the upper limit set at 50 u ml-1 and the peanut lectin assay improved the sensitivity to 85% with only a slight fall in specificity (85%). These results compare well with published results for ultrasound and CT scanning.
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PMID:Enzyme-linked PNA lectin binding assay compared with CA19-9 and CEA radioimmunoassay as a diagnostic blood test for pancreatic cancer. 273 32

Evidence is accumulating that colonic mucin glycoconjugates are altered in ulcerative colitis. In order to investigate this further, the lectin-binding properties of rectal glycoconjugates have been studied in ulcerative colitis, Crohn's disease, and controls using lectin-peroxidase histochemistry. Ten lectins were used including peanut agglutinin (PNA) which is known to bind to malignant and adenomatous but not normal colonic mucins. Eight of 21 ulcerative colitis rectal biopsies and 10 of 17 Crohn's disease rectal biopsies showed PNA positivity, particularly in the supranuclear region of surface epithelial cells. There was no correlation between PNA positivity and duration of disease or inflammation, and none of the biopsies showed evidence of dysplasia. This abnormality in epithelial cell glycoconjugates seems to be commonly present in nondysplastic mucosa and occurs in both ulcerative colitis and Crohn's disease. It may reflect a fundamental abnormality in mucus glycoprotein synthesis in inflammatory bowel disease.
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PMID:Altered lectin binding by colonic epithelial glycoconjugates in ulcerative colitis and Crohn's disease. 318 Sep 71

We have examined the ability of intestinal and peripheral blood mononuclear cells isolated from patients with inflammatory bowel disease to mediate killing against cell line targets in spontaneous, antibody-dependent, lectin-induced, and interferon-induced cell-mediated cytotoxicity assays, as well as responsiveness in the allogeneic mixed leukocyte reaction, and effector capabilities in cell-mediated lympholysis. IMC were poor mediators of spontaneous or antibody-dependent cellular cytotoxicity with cell line cells as targets (in comparison to normal PBMC, but were capable of killing antibody coated chicken red blood cells. Although IMC were capable of responding to allogeneic cell surface antigens in the mixed leukocyte reaction, they did not exhibit effector function in cell-mediated lympholysis. Mitogenic lectins induced cell-mediated cytotoxicity by isolated intestinal mononuclear cells from controls and patients. HFIF induces cytotoxicity by control but not inflammatory bowel disease intestinal cells. Pokeweed mitogen was the lectin which induced the greatest amount of killing against human cell line targets. We therefore speculate that exogenous agents, or endogenous factors released during viral infection, could play a role in inducing cell mediated cytotoxic damage to the intestine in inflammatory bowel disease patients. In addition, the functional differences between IMC and PBMC indicate that intestinal MNC may have unique cell capabilities which must be better understood prior to the delineation of immunopathologic events in solid organ tissues. We have also examined the secretion of IgA, IgM, and IgG by isolated human IMC, human bone marrow MNC from rib specimens, and PBMC from patients with CD, UC, SLE, or Henoch-Schoenlein purpura (HSP). Control IMC exhibited high spontaneous secretion of IgA, while intestinal MNC from UC and CD patients exhibited only modest increases in IgA secretion. PBMC from patients with CD, UC, SLE, or HSP exhibited markedly elevated spontaneous secretion of immunoglobulins in general and IgA in particular. Pure human bone marrow MNC exhibited high spontaneous secretion of IgA, and modest amounts of IgG and normal IgM secreting. The addition of PWM to cultures exhibiting high spontaneous synthesis and secretion of immunoglobulins resulted not in further enhancement but in suppression of antibody secretion. The characterization of types of IgA secreted by human IMC revealed that normal human bone marrow secretes almost exclusively monomeric IgA, while control human intestine secretes predominantly dimeric IgA. IMC from patients with CD and non-involved UC specimens also secreted predominantly dimeric IgA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Isolation and characterization of cytotoxic effector cells and antibody producing cells from human intestine. 387 4

Intestinal mononuclear cells are poor mediators of spontaneous and antibody-dependent cellular cytotoxicity. In this study, we found that both interferon and mitogenic lectins were able to induce increased levels of cell-mediated cytotoxicity by intestinal mononuclear cells. Intestinal mononuclear cells from patients with inflammatory bowel disease exhibited hyporesponsiveness to cytotoxic activation by interferon or lectins compared with control intestinal mononuclear cells. Peripheral blood mononuclear cells from patients with Crohn's disease exhibited deficient spontaneous and antibody-dependent cytotoxicity that could be partially reversed by interferon or mitogenic lectins. These studies demonstrate that exogenous agents or endogenous factors can induce deficient intestinal and peripheral blood cytotoxic effector cells from inflammatory bowel disease patients to become active. In comparison with control cells, however, intestinal and peripheral blood mononuclear cells from inflammatory bowel disease patients are not only deficient in cytotoxic capabilities but also are hyporesponsive to interferon and lectin activation.
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PMID:Deficient cell-mediated cytotoxicity and hyporesponsiveness to interferon and mitogenic lectin activation by inflammatory bowel disease peripheral blood and intestinal mononuclear cells. 394 Feb 56

Glycoconjugate composition of colorectal goblet cell mucin was characterized according to the anatomical distribution of lectin-binding sites in mucosal biopsies from 35 control subjects and 55 patients with inflammatory bowel disease. 24 of the controls had mucosal inflammation on biopsy, without clinical evidence of inflammatory bowel disease. These inflamed controls showed a similar rate of presence of lectin-binding sites as the normal noninflamed group. In the controls, the frequency of binding of Ricinus communis agglutinin I to galactosyl residues was consistently higher than that found with either Ulex europaeus agglutinin I to fucosyl or Dolichus biflorus agglutinin to N-acetyl galactosyl groups. A significant proximal to distal gradient for Ulex europaeus agglutinin I binding sites was identified in the controls group. These binding sites were present four times more often in the proximal colon than in the distal colon (P less than 0.025). In the ulcerative and Crohn's colitis groups, this gradient effect was lost, predominantly as a result of decreased availability of fucosyl residues in the proximal colon. In the descending colon of Crohn's colitis tissues, there was a complete absence of Dolichus biflorus agglutinin binding sites compared with the 62.5% incidence in the control group (P less than 0.05). These results demonstrate that the expression of lectin-binding sites in human large intestinal goblet mucin is specifically altered in inflammatory bowel disease, indicating that there are changes in glycosylation of colorectal mucin consistent with alterations in goblet cell differentiation.
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PMID:Regional distribution and alterations of lectin binding to colorectal mucin in mucosal biopsies from controls and subjects with inflammatory bowel diseases. 396 99


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