Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gastric spirillum Helicobacter felis, originally isolated from the cat stomach, colonizes the stomachs of germfree rats. Studies were designed to examine the pathological and serological responses of germfree rats inoculated orally with H. felis. At 2 weeks postinoculation, the gastric mucosa of germfree rats had lymphocytes and eosinophils scattered in small foci throughout the subglandular region of the antrum. Small numbers of lymphocytes were present in the subglandular portion of the antral mucosa that focally extended through the lamina propria towards the luminal surface. Eight weeks postinoculation, the inflammation was confined to the antrum. It was characterized by increased numbers of lymphocytes and eosinophils in the subglandular areas, with focal aggregates of lymphocytes in the submucosa. Some lymphoid aggregates extended from the submucosa through the muscularis mucosa and lamina propria to the luminal surface. H. felis was demonstrated with the Warthin-Starry stain, bacterial culture, and urease assay, particularly in the antrum. H. felis also produced a significant immunoglobulin G antibody titer at 2, 4, and 8 weeks postinoculation as well as a transitory immunoglobulin M response at 2 to 4 weeks postinoculation. Contact control rats were not infected, inferring that fecal-oral spread of H. felis did not occur.
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PMID:Helicobacter felis gastritis in gnotobiotic rats: an animal model of Helicobacter pylori gastritis. 199 30

Numerous reports have established the association of Helicobacter pylori and peptic ulcer disease in adults. Recently, this association has also been demonstrated in children. We investigated 14 children and adolescents with recurrent abdominal pain. In six patients, endoscopy revealed gastritis and Helicobacter pylori was identified. Giemsa stain was more sensitive than culture or urease testing in identifying the bacteria. In four of the six, a nodular appearance of the antral mucosa was observed. The histological examination suggests lymphoid hyperplasia as the cause of the nodularity. All of the patients became symptomless after combined treatment with amoxicillin and bismuth subsalicylate. We conclude that nodular gastritis is a peculiar type of gastritis in children. It is frequently found in association with Helicobacter pylori infection.
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PMID:Nodular gastritis and Helicobacter pylori. 205 Dec 85

Recently, a close relation has been found between infection of the gastric mucosa by Campylobacter pylori and chronic gastritis. To establish the possible existence of characteristic morphologic changes in this disease, which can be differentiated from other unrelated forms of gastritis, we analyzed the antral biopsies obtained from 75 patients, 35 with duodenal peptic ulcer and 40 with nonulcerous dyspepsia. The diagnosis of C. pylori infection is based on positive biopsy culture or, if not, when following three requirements are met: positive urease test before 24 hours, identification of the germ by Gram stain and visualization in the tissue of microorganisms with morphology similar to that of C. pylori. We found that 85.5% of the 55 patients with C. pylori infection present active chronic gastritis with lymphoid nodes (GCA + NL), while this morphology is only found in 5 of the 20 uninfected patients. The association of GCA + NL with C. pylori infection is highly significant (p less than 0.0001). We think that it could be a local immunologic response to the stimulus of the bacterial antigen, and that it has sufficient morphologic entity to differentiate it from other inflammatory processes of the gastric mucosa of still unknown etiology.
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PMID:[Morphology of chronic gastritis associated with Campylobacter pylori infection]. 262 10

UV irradiation is known to photoisomerize epidermal trans-urocanic acid (trans-UCA) to cis-urocanic acid (cis-UCA), which has been postulated to be involved in local and systemic downregulation of immune responses. We have earlier shown that cis-UCA suppresses interleukin 1 (IL-1) production in human epidermal cells. To study the possible effects of UCA isomers on human peripheral blood lymphoid cells, these cells were cultured in the presence of either UCA stereoisomer, and a number of immunological parameters were assayed. Cis-UCA (100 micrograms/ml) caused a significant downregulation of monocyte IL-1 production, and diminished monocyte HLA-DR expression. Cis-UCA also caused a significant reduction in the CD4/CD8 ratio. Furthermore, T-cells preincubated with cis-UCA caused a significant downregulation of purified protein derivative-induced interleukin 2 production by autologous T-cells. The trans isomer had no effect in any of these in vitro tests. The reported stereospecific effects of cis-UCA are compatible with the postulated function of this chemical as an UV-induced, low-molecular-weight immunomediator substance.
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PMID:Cis-urocanic acid stereospecifically modulates human monocyte IL-1 production and surface HLA-DR antigen expression, T-cell IL-2 production and CD4/CD8 ratio. 263 83

The endoscopic picture of peptic ulcer was studied in 104 patients; the gastric mucosa of 30 per cent of the patients was infected with Campylobacter pyloridis (CP) and had acute erosions in the pyloroduodenal zone. Erosions in uninfected patients were found in 3 per cent of the cases. The predominant lymphoid infiltration of the mucous coat of the stomach was revealed in 60 ulcer patients irrespective of the CP infection. Mucous infiltration with polymorphonuclear leukocytes was found in 13 chronic gastritis patients (in 6 of them gastritis was combined with CP infection). The urease test was positive during the first hour in 82 per cent of the cases in the presence of a large number of CP in histological specimens. Treatment of 31 patients with gastric campylobacteriosis using various antibacterial agents or their combination revealed that continuous 2 months bismuth subnitrate medication was more effective for gastric mucosa disinfection. In addition, favourable results were often obtained when a combination of two antimicrobial agents was used.
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PMID:[Diagnosis and treatment of gastric campylobacteriosis in patients with peptic ulcer and chronic gastritis]. 271 60

In order to understand the relation between the prevalence of Campylobacter pylori and the severity of gastritis, we conducted a survey of 166 randomly selected dyspeptic patients. The presence of C. pylori on the antral mucosa was aseptically determined by both urease and bacterial culture tests. Specimens of antral mucosa were obtained for pathologic gradings of inflammation: active gastritis, mononuclear cell infiltration C0 (nil) to C3 (lymphoid follicle); presence or absence of intestinal metaplasia. Pathologically, chronic gastritis was invariably present in almost all patients with dyspepsia: three-fourths of them showed evidence of active gastritis, one-third showed intestinal metaplasia. Half of the dyspeptic individuals had C. pylori colonization. The results suggest that the prevalence of C. pylori was closely related to the different grades of active gastritis; neither the different grades of chronic gastritis nor intestinal metaplasia affected the prevalence of C. pylori on gastric mucosa. We conclude from this study that C. pylori is closely related to active chronic gastritis because of the common presence of chronic gastritis in patients with dyspepsia.
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PMID:The relation between Campylobacter pylori and inflammatory cell infiltration of antral mucosa in patients with dyspepsia. 275 23

Twenty-four young adult domestic cats from a commercial vendor were found to be infected with Helicobacter pylori. Histopathologic analyses, selected electron microscopy, and urease mapping were performed on mucosal samples collected from the cardias and fundi, bodies, and antra of these cats' stomachs. H. pylori organisms were abundant in all areas of the stomach on the basis of histologic evaluation and urease mapping. H. pylori infection was associated with a moderate to severe lymphofollicular gastritis in 21 of 24 cats (88%). The gastritis was most pronounced in the antral region and consisted mainly of multifocal lymphoplasmacytic follicular infiltrates in the deep mucosa. The severity of gastritis in the antrum corresponded to high numbers of H. pylori there on the basis of the use of the urease assay as an indicator of H. pylori colonization. Ten of 24 cats (42%) also had small to moderate numbers of eosinophils in the gastric mucosa. All 24 cats had gastric lymphoid follicles, with follicles being most prevalent in the antrum. Electron microscopy of gastric tissue revealed numerous H. pylori organisms, some of which were closely adhered to the mucosal epithelium. Human H. pylori gene-specific primers to ureA and ureB amplified products of similar sizes from H. pylori cat isolates. Digestion of the products with restriction enzymes resulted in fragments characteristic of the restriction fragment length polymorphism patterns of H. pylori isolates from humans. In the domestic cat, H. pylori infection is associated with a lymphofollicular gastritis, consisting of lymphocytic and plasmacytic infiltration into the lamina propria, and the organism appears to provide chronic antigenic stimulation resulting in the formation of gastric lymphoid follicles.
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PMID:Characterization of feline Helicobacter pylori strains and associated gastritis in a colony of domestic cats. 749 15

The ability of oral immunization to interfere with the establishment of infection with Helicobacter felis was examined. Groups of Swiss Webster mice were immunized orally with 250 micrograms of Helicobacter pylori recombinant urease (rUrease) and 10 micrograms of cholera toxin (CT) adjuvant, 1 mg of H. felis sonicate antigens and CT, or phosphate-buffered saline (PBS) and CT. Oral immunization with rUrease resulted in markedly elevated serum immunoglobulin G (IgG), serum IgA, and intestinal IgA antibody responses. Challenge with live H. felis further stimulated the urease-specific intestinal IgA and serum IgG and IgA antibody levels in mice previously immunized with rUrease but activated primarily the serum IgG compartment of PBS-treated and H. felis-immunized mice. Intestinal IgA and serum IgG and IgA anti-urease antibody responses were highest in rUrease-immunized mice at the termination of the experiment. Mice immunized with rUrease were significantly protected (P < or = 0.0476) against infection when challenged with H. felis 2 or 6 weeks post-oral immunization in comparison with PBS-treated mice. Whereas H. felis-infected mice displayed multifocal gastric mucosal lymphoid follicles consisting of CD45R+ B cells surrounded by clusters of Thy1.2+ T cells, gastric tissue from rUrease-immunized mice contained few CD45R+ B cells and infrequent mucosal follicles. These observations show that oral immunization with rUrease confers protection against H. felis infection and suggest that gastric tissue may function as an effector organ of the mucosal immune system which reflects the extent of local antigenic stimulation.
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PMID:Effect of oral immunization with recombinant urease on murine Helicobacter felis gastritis. 789 Mar 80

The treatment of peptic ulcers has been revolutionized by the discovery that Helicobacter pylori (H. pylori) bacteria is a causative agent for ulcer formation. However, when patients present with dyspepsia or epigastric discomfort, more than 80% of patients will not have ulcer disease and empiric treatment of H. pylori is not recommended for these patients. Eradication of H. pylori has not been demonstrated to improve the symptoms of non-ulcer dyspepsia compared with non-ulcer dyspepsia patients treated with placebo. Therefore, we recommend that patients should first be evaluated for peptic ulcers with endoscopy or upper gastrointestinal series before the diagnosis and treatment of H. pylori. Generally, the treatment of H. pylori should be limited to patients with peptic ulcers, mucosal-associated lymphoid tissue lymphomas, and gastric cancers. Most diagnostic tests for H. pylori, including quantitative IgG antibody, urea breath tests, rapid urease tests (CLO), tests of gastric mucosal biopsies, and staining of gastric mucosal biopsies, have equivalent diagnostic characteristics. Therefore, the choice of diagnostic test for H. pylori should be based on cost, ease of use, and lack of complications. Multiple antibiotic regimens are available for the treatment of H. pylori. Triple antibiotic therapy is the least expensive but has the highest rate of side effects and the least compliance. Combining a proton pump inhibitor with clarithromycin and another antibiotic will eradicate H. pylori with fewer side effects and better compliance but this is the most expensive antibiotic regimen.
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PMID:Acid peptic diseases in the era of Helicobacter pylori. 970 81

While European and United States guidelines for the management of Helicobacter pylori infection have been developed, there are no guidelines for the Asian Pacific. International experts and recognised local authorities met in Singapore in 1997 to develop appropriate guidelines, taking into account the high background prevalence of infection, high incidence rates of gastric cancer and resource limitations. Recommendations were made based on randomised controlled trials or where this was not possible, they were based on the current best available evidence or on good clinical practice. A number of acceptable diagnostic tests for infection are available throughout the region. The non-endoscopic methods of choice are the urea breath test or a locally validated antibody test. If endoscopy was to be performed, a biopsy urease test was recommended as the test of first choice, with histology recommended only if this was negative. Post treatment testing was not recommended for all patients; a urea breath test was considered the test of choice if available. All gastric and duodenal ulcer patients who are infected with H. pylori should be treated for H. pylori whether the ulcer is active or in remission. Patients requiring long term non-steroidal anti-inflammatory drug therapy who have a current or recent history of dyspepsia, patients with early gastric cancer or low grade gastric mucosa associated lymphoid tissue lymphoma, and patients with a family history of gastric cancer should be treated. However, it was concluded that there wasn't sufficient evidence that cure of H. pylori infection reduces the risk or prevents the development of gastric adenocarcinoma. Many patients with dyspepsia in the region will request or require early upper endoscopy because of an inherent fear of gastric cancer. However, where endoscopy is not available or is too costly, alternative acceptable approaches were recommended in high risk cancer regions. While evidence is inconclusive to support treatment of H. pylori infection in non-ulcer dyspepsia, it was agreed that treatment be offered to patients with documented infection on a case-by-case basis. Treatment regimens need to attain an eradication rate of 90% or greater by per protocol analysis and 80% or greater by intention-to-treat analysis. A number of 7-day regimens were recommended based on available evidence. These regimens were considered likely to maximize the chances of successful eradication with one course of treatment, thereby reducing the risk of acquired antibiotic resistance and leading to long term cost savings.
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PMID:Report of the 1997 Asia Pacific Consensus Conference on the management of Helicobacter pylori infection. 973 64


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