Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009324 (ulcerative colitis)
 17,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Invasive Escherichia coli strains of certain serotypes invade by the same mechanism as the Shigella sp. It has been proposed that invasion of epithelial cells by EPEC strains may also occur; this is a previously overlooked property. In the present study E. coli strains isolated from patients with diarrhoea or ulcerative colitis, lacking the inv plasmid mediating classical invasion, but hybridizing with probes for different adhesins, were analyzed for their ability to invade HeLa and Caco-2 cells. The majority of strains invaded Caco-2 cells to a higher extent than HeLa cells. Adhesion to Caco-2 cells was a prerequisite for subsequent invasion of the cells but EAF, eae, EAgg and other known virulence factors were not sufficient to mediate invasion. In 8/9 E. coli strains invasion was enhanced after growth under iron restriction. Growth during anaerobic conditions did not influence subsequent invasion by E. coli strains whereas 6/9 strains had their invasive ability significantly decreased after growth in the presence of 1% glucose. The invasive process was inhibited by mannose but not by lactose, fucose or galactose. Our data indicate that strains of E. coli may invade Caco-2 cells by novel mechanisms which require adhesion to the cells but which differ from those of Salmonella sp., Yersinia sp., Shigella sp. and classical enteroinvasive E. coli.
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PMID:Invasion of tissue culture cells by diarrhoeagenic strains of Escherichia coli which lack the enteroinvasive inv gene. 880 71

Anti-neutrophil cytoplasm antibodies (ANCA) have been found in the sera of patients presenting systemic necrotizing microscopic vasculitis, i.e. Wegener's granulomatosis and microscopic polyangiitis. Lactoferrin (LF) is one of the antigens rarely recognized by ANCA, and anti-LF autoantibodies are found in several autoimmune conditions, including rheumatoid vasculitis, rheumatoid arthritis, systemic lupus erythematosus, ulcerative colitis, primary sclerosing cholangitis and Crohn's disease. We analysed the epitopes recognized by human anti-LF antibodies to test whether the heterogeneity of clinical presentation might be due to a different epitope recognition profile. Several monoclonal antibodies were raised and used in competition studies with six human sera. Four distinct epitopes were identified on LF, and LF binding of only one of six sera was inhibited by one of the monoclonals. Thus, anti-LF autoreactivity appears to be polyclonal and not restricted to an immunodominant epitope. Specific epitope profiles cannot be determined in these autoimmune conditions. We hypothesized that the interaction of anti-LF antibodies with the LF iron binding domain might contribute to pathogenesis by inhibiting iron chelation after neutrophil activation, thereby providing increased iron availability for endothelial cell damage. The relation of anti-LF mouse monoclonals or polyclonal human or rabbit antibodies to the LF iron-binding domain was studied in competition assays between 59Fe and these antibodies. Preincubation of LF with monoclonals or anti-LF human sera did not affect the binding of 59Fe on LF. 59Fe-binding kinetic studies showed that rabbit anti-LF polyclonal, but not mouse monoclonals or human anti-LF positive sera, was capable of inhibiting iron binding on LF. Therefore, anti-LF autoantibodies did not appear to modulate LF iron-binding activity. We conclude that LF is a rare antigen specificity for ANCA and that the clinical and pathophysiological relevance of anti-LF autoreactivity remains uncertain.
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PMID:Anti-lactoferrin autoantibodies: relation between epitopes and iron-binding domain. 886 34

Lactoferrin (LF) is an iron binding protein, which may represent a target for antineutrophil cytoplasmic antibodies (ANCA) in patients affected by rheumatoid arthritis, ulcerative colitis, and primary sclerosing cholangitis. Here we describe the production and characterization of two new monoclonal antibodies (MAbs) against human LF. These MAbs (AGM 10.14, an IgG1, and AGM 2.29, an IgG2b) recognize spatially distant epitopes of LF as assessed by cross-blocking experiments. We also demonstrated by indirect immunofluorescence that both MAbs react with ethanol-fixed neutrophil granulocytes showing a perinuclear staining pattern. AGM 2.29 and AGM 10.14 have been utilized as capture and labeled tracer antibody, respectively, in a double determinant immunoassay (DDIA) to measure soluble LF. The results obtained show that this DDIA allows us to quantify even low concentrations of LF, the maximal range of the assay sensitivity being between 12 and 780 ng/ml. Therefore, AGM 10.14 and AGM 2.29 may represent useful reagents for studying the role of autoantibodies to LF as well as for measuring soluble LF, which is a reliable secretory marker of neutrophil activation.
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PMID:Two spatially distant epitopes of human lactoferrin. 888 Feb 13

Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation whose cellular components are capable of oxidative respiratory bursts that may result in tissue injury. Mucosal biopsies were analyzed for protein carbonyl content (POPs), DNA oxidation products [8-hydroxy-2'-deoxyguanosine (8-OHdG)], reactive oxygen intermediates (ROIs), trace metals (copper, zinc, and iron) and superoxide dismutase (Cu-Zn SOD). In Crohn's disease biopsies, there was an increase in ROIs, POPs, 8-OHdG, and iron, while decreased copper and Cu-Zn SOD activity were found in inflamed tissues compared to controls. For ulcerative colitis, there was an increase in ROIs, POPs, and iron in inflamed tissue compared to controls, while decreased zinc and copper were observed. An imbalance in the formation of reactive oxygen species and antioxidant micronutrients may be important in the pathogenesis and/or perpetuation of the tissue injury in IBD and may provide a rationale for therapeutic modulation with antioxidants.
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PMID:Increased oxidative stress and decreased antioxidant defenses in mucosa of inflammatory bowel disease. 888 24

Leukocyte scintigraphy (LS) was performed in 20 pediatric patients with inflammatory bowel disease (IBD: 10 with ulcerative colitis, 2 with indeterminate colitis, and 8 with Crohn disease) in different stages of clinical activity. Leukocytes were separated from 15 to 60 ml venous blood and were labeled in vitro with [99mTc]HM-PAO. The segmental extent (small intestine; ascending, transverse, and descending colon; and recto-sigmoideum) of the process was determined by LS. The uptake of each bowel segment was scored in relation to the bone marrow uptake. The scintigraphic activity, calculated by summing the segment scores, was compared with laboratory parameters. The mean labeling efficacy was 76% (60-86%). The segmental extent of the process determined by LS was compared with the results of barium enema or colonoscopy with regard to 32 bowel segments. The sensitivity, specificity, and accuracy of LS were 93, 88, and 91%, respectively. Two extraintestinal manifestations (abdominal abscess and joint involvement) were also detected by LS. These lesions were verified by computed tomography (CT) (abscess) and on the basis of the clinical outcome (arthritis). The scintigraphic activity correlated with the C-reactive protein (CRP) level (r = 0.82, p < 0.001), the alpha 2-globulin level (r = 0.63, p < 0.02), the sedimentation rate (r = 0.51, p < 0.05), and the fS iron level (r = -0.66, p < 0.005). LS is applicable in pediatric patients. The method is an excellent technique for assessment of the extent of IBD in children. Extraintestinal manifestations of IBD can also be investigated by LS. The scintigraphic activity is a useful parameter for determination of the activity of IBD in children.
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PMID:HM-PAO-labeled leukocyte scintigraphy in pediatric patients with inflammatory bowel disease. 898 43

Ulcerative colitis is a chronic inflammatory disease of the colon where leukotrienes are suggested to play an important role for keeping inflammation active. Boswellic acids, the biologically active ingredients of the gum resin of Boswellia serrata (Sallai guggal), have been shown to be specific, nonredox and noncompetitive inhibitors of 5-lipoxygenase, the key enzyme of leukotriene biosynthesis. In patients suffering from ulcerative colitis grade II and III the effect of Boswellia serrata gum resin preparation (350 mg thrice daily for 6 weeks) on stool properties, histolopathology and scan microscopy of rectal biopsies, blood parameters including Hb, serum iron, calcium, phosphorus, proteins, total leukocytes and eosinophils was studied. Patients receiving sulfasalazine (1 g thrice daily) served as controls. All parameters tested improved after treatment with Boswellia serrata gum resin, the results being similar compared to controls: 82% out of treated patients went into remission; in case of sulfasalazine remission rate was 75%.
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PMID:Effects of Boswellia serrata gum resin in patients with ulcerative colitis. 904 93

Various genera of sulphate reducing bacteria (SRB) have been found in the human digestive tract. It is suggested that some of SRB species may be responsible for the development of the clinical symptoms of ulcerative colitis and other disease of large intestine. Sulphasalazine (salicyl-azo-sulphapyridine, SAS) is commonly used to treat patients with ulcerative colitis and Crohn disease. Above 30 samples of faeces or biopsy specimens from 25 patients (age 45 +/- 14 years; M/F, 13/12) suffering from gastrointestinal disorders were used for isolation of Desulfovibrio desulfuricans species. The morphological, physiological and biochemical characteristics of isolated strains and also their susceptibility to SAS was determined. D. desulfuricans isolates were obtained from 5 amongst all patients assayed. Some abnormal, cigar-shaped cells were detected as accompanying the cells represented by rods, curved rods and vibrios. After strains purification, two types of colonies were present on the solid Postgate's medium B (containing lactate as a carbon source and sulphate for energy conservation): the black colonies growing in bulk of agar medium and the transparent, surface-growing mucous colonies. These two types of D. desulfuricans colonies may be a result of different iron availability for bacterial cells. High metabolic activity of strain was not always accompanied by the presence of H2S gas lock in the test tube, although the H2S odor was perceptible. All tested strains multiplied inconsiderably slowly in the presence of SAS at concentrations 10, 20, 40 and 60 mg/cm3. The growing concentrations of SAS did not cause a proportional decrease of the bacterial cells number. Taking into account the positive results of using SAS to treat patients with some colonic diseases and the indicated resistance to SAS of intestinal D. desulfuricans strains, it appears probable, that this SRB species isn't responsible for the development of mentioned diseases.
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PMID:Isolation and evaluation of susceptibility to sulphasalazine of Desulfovibrio desulfuricans strains from the human digestive tract. 942 89

Depletion of goblet cells (the main mucin-producing cells in the colon) is one of the most reliable histological characteristics of ulcerative colitis, whereas a major symptom of this disease is bloody diarrhea containing a large amount of mucus. The discrepancy between these phenomena was investigated in a time-course study in rats with experimental colitis induced by treatment with oral dextran sulfate sodium (DSS) for 1, 3, or 5 days. Biochemical analysis showed a reduction in mucin content in the distal side of the colon that was proportional to the duration of DSS administration. In the proximal side of the colon, however, there was a significant increase in mucin content already on the first day of treatment with DSS. This increase in colonic mucin content continued for the 5 days of treatment. In the distal side, both sulfomucin and sialomucin decreased proportionally to the duration of DSS administration. In the proximal side, there was an increase in high iron diamine-Alcian blue-positive mucins, and confirming the proliferation of goblet cells. The proliferated glands were predominantly sialylated. Goblet cell depletion and an increase in mucin production occurred in different parts of the colon. This phenomenon may be a type of compensatory function of colon tissue in response to the localized decrease of mucin production in certain portions of the colon.
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PMID:Compensatory response of colon tissue to dextran sulfate sodium-induced colitis. 1021 20

Adenocarcinoma arising at an ileostomy is uncommon, and only 29 cases have been reported in the literature. The case of a 54-year-old man who developed an adenocarcinoma at a Brooke ileostomy is reported. The ileostomy had been fashioned 21 years earlier after proctocolectomy for familial adenomatous polyposis (FAP). A wide local excision of the stoma was performed, and a new Brooke ileostomy was fashioned on the opposite side of the abdomen. Histopathologic examination revealed a well-differentiated adenocarcinoma with early invasion of the submucosa. On hematoxylin and eosin staining, the ileal mucosa adjacent to the tumor showed signs of colonic metaplasia, including loss of villous architecture and a reduced number of Paneth cells. Mucin staining using the high iron diamine-alcian blue stain demonstrated a mixture of sulfomucin and sialomucin in the ileal mucosa near the tumor, confirming colonic metaplasia. Ileostomy site carcinogenesis can be attributed to both the colonic metaplasia and the inherent nature of FAP or ulcerative colitis (UC), where colonic mucosa is susceptible to adenoma formation or dysplasia. Longstanding ileostomies in patients with FAP or UC should be followed to exclude the development of adenoma, dysplasia, or cancer.
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PMID:Familial adenomatous polyposis: a case report and histologic mucin study. 1037 42

Ulcerative colitis (UC) and, to a lesser extent, Crohn's disease (CD) are associated with a reduction of the protective mucus layer in the large intestine; the role of this alteration in the pathogenesis of either disease is, however, not clear. To learn more about the molecular mechanism of the alteration of the mucus layer, the expression of the main intestinal mucin, MUC2, was investigated in relation to inflammation and dysplasia. Formalin-fixed, paraffin-embedded biopsies from 70 patients with UC and 16 patients with CD, and 13 biopsies from normal colonic mucosa, were used for detection of MUC2 mRNA by in situ hybridization with the SMUC41 probe, and MUC2 protein by immunohistochemistry with the antibody CCP58. The steady-state concentration of MUC2 mRNA was not affected by UC or CD. By contrast, the amount of the detectable MUC2 protein, assessed as the immunoreactive score (IRS), was significantly (p<0. 0001) increased in UC (IRS=8.0+/-3.8) and CD (8.0+/-3.7), compared with the normal colonic mucosa (IRS=2.0+/-1.5). This alteration occurred in the inactive phase of inflammation and persisted in the active phase of the disease. It was also observed during bacterial or protozoal inflammation (n=7). The IRS values did not correlate with the grade of inflammation or dysplasia. Simultaneous histochemistry with high iron diamine and immunohistochemistry indicated that the increase of detectable MUC2 is concomitant with low mucin sulphation in the same cells. These data indicate that the strong MUC2 protein staining in colonic mucosa of patients with UC or CD is due to a long-term alteration of the post-transcriptional modification of the MUC2 molecule, leading to its better detectability by the anti-MUC2 antibody CCP58. This alteration, induced by the inflammatory process, may affect the gel thickness and may contribute to a protracted autoimmune response.
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PMID:Defective post-transcriptional processing of MUC2 mucin in ulcerative colitis and in Crohn's disease increases detectability of the MUC2 protein core. 1041


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