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)

Enzyme-linked immunosorbent assays (ELISAs) have been developed to diagnose Helicobacter pylori infection. However, the methods are not standardized. We therefore prospectively evaluated the sensitivities and specificities of ELISAs developed in the United States and the United Kingdom in a study population comprising 41 consecutive symptomatic outpatients and 35 volunteers. At endoscopy, multiple biopsies were obtained for histology and culture and stained sections were graded for chronic gastritis, active chronic gastritis, and density of H. pylori. Serum samples were analyzed for H. pylori by ELISA. The first set of assays for immunoglobulin G (IgG) and IgA used a pool of sonicated isolates of H. pylori from five patients in the United States (antigen A). The second set of assays, developed in the United Kingdom, used three different antigens: antigen 1, an acid-extractable surface antigen; antigen 2, an acid-extractable antigen from an aflagellate variant; and antigen 3, a urease-containing fraction. Cutoff scores for positive results were determined a priori on the basis of previous serological studies. There was close agreement between histology and culture. In the study population, 36% of the individuals were H. pylori positive. The diagnostic value of the different ELISAs were highly comparable, and the crude antigens performed as well as the more purified antigens. The antigen A IgG had a sensitivity and specificity of 96 and 94%, respectively; the values for antigen 1 were 93 and 96%, respectively. The antigen A IgA and antigen 3 assays were the least sensitive tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serodiagnosis of Helicobacter pylori: comparison of enzyme-linked immunosorbent assays. 176 85

Helicobacter pylori can be considered a very successful organism effectively colonizing the majority of the world's population. Although various disease states associated with this infection have been described, the mechanisms of pathogenicity remain unknown. The easiest virulence factors to identify are those enabling the organism to colonize the hazardous microenvironment of the gastric epithelium, survive at this site, and multiply sufficiently for transmission to a new host. The factors identified to date include the bacterial enzymes urease and catalase, flagella, and lectin-like adhesins. In addition, it is proposed that the organism has evolved mechanisms to avoid the local antibody responses of the host. Several putative virulence factors that could directly cause gastroduodenal damage have also been identified. These include the direct tissue damage by cytotoxins or the products of urease activity and the indirect tissue damage due to disruption of mucin integrity. Such mechanisms may contribute to peptic ulcer formation; however, the chronic superficial gastritis most frequently associated with this infection is probably caused by immunopathologic events mediated by the host in response to the continued antigen load on the gastric mucosa.
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PMID:Virulence factors of Helicobacter pylori. 177 22

Urease (urea amidohydrolase, EC 3.5.1.5) catalyzes the hydrolysis of urea to yield ammonia and carbon dioxide. Research on this enzyme has gained momentum since the discovery of Helicobacter pylori as a causative agent of human gastritis. The remarkably high urease activity of each organism has served as the basis of diagnostic tests for the presence of the organism in the urease biopsy test and urea breath test. Urease undoubtedly plays a central role in H. pylori pathogenesis. Hydrolysis of urea with generation of ammonia may enable survival of this acid-sensitive organism in the gastric mucosa. Ammonia generated by urea hydrolysis may also produce severe cytotoxic effects within gastric epithelium. The enzyme also elicits a strong immune response during acute infection, suggesting that this abundant antigen is readily available to the immune system. An increase in serum IgG titer is predictive of ongoing infection. Much progress has been made with regard to the molecular biology of urease. The high molecular weight protein (estimated by several investigators to be 300-520 kDa) has been purified, revealing two distinct subunits of 29.5 kDa and 66 kDa, a unique subunit structure as compared with other microbial ureases. However, amino acid sequences are nevertheless well conserved when compared with other bacterial ureases and that of the jack bean, Canavalia ensiformis. Furthermore, genes encoding urease of H. pylori have been cloned, sequenced, and amplified by the polymerase chain reaction.
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PMID:Helicobacter pylori urease: properties and role in pathogenesis. 177 23

Twenty-one patients with endoscopically confirmed duodenal ulceration, who had failed to heal with an H2-antagonist, were given omeprazole 20 mg o.m. for four weeks. Four antral biopsies from each patient were taken at endoscopy before, at the end of, and four weeks after treatment. Rapid urease test, culture, histopathology and transmission electron microscopy were carried out on these biopsies to determine the presence of Helicobacter pylori and improvement of gastritis. After four weeks of treatment, duodenal ulceration was healed in 16 (79%) of the patients; H. pylori was not detected by culture in 11 (50%) of the patients, and the associated gastritis improved in 12 (54%) patients. Four weeks after cessation of treatment the organism was cultured from antral biopsies of 18 (86%) of the patients and all of these had gastritis. Omeprazole treatment healed duodenal ulceration, improved gastritis temporarily, and suppressed but did not eradicate H. pylori.
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PMID:Short report: the effect of omeprazole on Helicobacter pylori and associated gastritis. 177 52

Helicobacter pylori (HP) is an important etiological factor in chronic gastritis and duodenal ulceration. Demonstration of HP by means of culture and histological examination is relatively time-consuming. The object of this investigation was to assess the validity of two rapidly read chemical tests: the buffered urease reagent (BR) and the unbuffered urease reagent (UBR) in demonstration of HP among patients referred for gastroscopy on account of upper abdominal dyspepsia. In 230 sets of biopsies investigated for HP by culture and histology, the following results were obtained by reading of the BR test three hours later at room temperature: Nosographic sensitivity 0.54, nosographic specificity 0.97, PVpos 0.93 and PVneg 0.71. In another material consisting of 57 sets of biopsies, both BR and UBR were performed. Reading of UBR after 15 minutes yielded the following results: Nosographic sensitivity 0.56, nosographic specificity 1.00, PVpos 1.00 and PVneg 0.61. It is concluded that positive results of the urease tests indicate the presence of HP. If the urease tests are negative, supplementary culture and/or histological examination for HP should be performed. UBR is preferable rather than BR.
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PMID:[Urease test for rapid demonstration of Helicobacter pylori in biopsies from the pyloric antrum]. 178 Oct 60

The purpose of the communication is to review the different aspects of the Helicobacter (Campylobacter) pylori infection. The first part of the communication is devoted to the description of the different gastric pathologies induced by the Helicobacter pylori infection and to the different methods used for the detection of this infection. Today a consensus assesses a causal role to Helicobacter pylori in the development of chronic active gastritis (or type B gastritis), in the pathogenesis of duodenal ulcer, and a major contributing factor in the development of peptic ulcer disease. The possible role played by this bacterium in the development of non-ulcer dyspepsia is still unclear. H. pylori infections can be detected using different methods including invasive methods--requiring an endoscopy (e.g.: culture of the micro-organism, urease test, microscopy) and non-invasive methods (e.g.: breath test, serology). Each of these methods has advantages but also some disadvantages, and none shows an absolute sensitivity and specificity. The second part of the presentation analyses the results obtained with a serologic method using a specific fractioned and purified antigenic complex extracted from Helicobacter pylori. This report demonstrates a good correlation with the other detection methods. Serology appears also as a useful tool for the therapeutical monitoring of infected patients. Serological results must however be interpreted in the light of the complete clinical examination of the patient.
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PMID:[The role of serology in the diagnosis of Helicobacter (Campylobacter) pylori infection]. 180 38

1. The demonstration of the association of H. pylori with gastritis and peptic ulcer has been of increasing interest to gastroenterologists, microbiologists, and histopathologists. 2. In this study, the presence of H. pylori in the gastric mucosa of children was investigated by culture, preformed urease test, and carbolfuchsin staining of biopsy smears. 3. The organism was detected in 44.9% of the children studied, and found to be distributed equally on the antral and fundic mucosa. 4. Compared to culture, the urease test and carbolfuchsin staining proved to be of higher sensitivity and specificity in detecting H. pylori.
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PMID:Diagnosis and distribution of Helicobacter pylori in the gastric mucosa of symptomatic children. 182 29

Fifty dyspeptic patients with histologically proven chronic superficial antral gastritis were treated for 6 weeks, in a randomized single-blind study, with esaprazole (450 mg bid) or sulglicotide (200 mg tid). Both drugs significantly improved the symptomatic score after 3 and 6 weeks (p less than 0.01), and the percentual rate of improvement was similar in the two groups studied. Similarly, both treatments significantly reduced the inflammation of gastric mucosa. Drugs were ineffective in clearing Helicobacter pylori from the antral mucosa (as assessed by the urease test, performed at entry and after 6 weeks). No side effects occurred after esaprazole or sulglicotide administration. The results of the present study suggest that esaprazole, a new gastroprotective drug, may have a role in the therapy of dyspeptic patients with chronic superficial gastritis.
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PMID:[Esaprazole vs sulglicotide in the treatment of dyspeptic patients with chronic superficial gastritis of the antrum]. 182 8

The inflammatory lesions associated with Helicobacter pylori gastritis and duodenitis contain large numbers of mononuclear cells. The close proximity of H. pylori to gastric mucosa suggests that the organism interacts with mononuclear cells, thereby modulating the inflammatory response. To investigate the role of monocytes/macrophages in this response, we examined the effect of whole H. pylori bacteria, H. pylori surface proteins, and H. pylori lipopolysaccharide (LPS) on purified human monocytes. Whole H. pylori and the extracted LPS induced expression of the monocyte surface antigen HLA-DR and interleukin-2 receptors, production of the inflammatory cytokines interleukin 1 and tumor necrosis factor (peptide and messenger RNA), and secretion of the reactive oxygen intermediate superoxide anion. Since H. pylori in vivo does not invade mucosal tissue, we determined whether soluble constituents of the bacteria could activate monocytes. Soluble H. pylori surface proteins, which are enriched for urease and do not contain LPS, stimulated phenotypic, transcriptional, and functional changes consistent with highly activated monocytes. These findings indicate that H. pylori is capable of activating human monocytes by an LPS-independent as well as an LPS-dependent mechanism. H. pylori activation of resident lamina propria macrophages and monocytes trafficking through the mucosa, leading to the secretion of increased amounts of inflammatory cytokines and reactive oxygen intermediates, could play an important role in mediating the inflammatory response associated with H. pylori gastritis and duodenitis.
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PMID:Soluble surface proteins from Helicobacter pylori activate monocytes/macrophages by lipopolysaccharide-independent mechanism. 184 39

Helicobacter pylori (formerly Campylobacter pylori) is the causative agent of gastritis in man. Helicobacter pylori cells contain a large amount of an extremely active urease (E.C.3.5.1.5). This enzyme is suspected to be a virulence factor since the ammonium ion produced from urea may be responsible for tissue injury and/or survival of H. pylori in the gastric environment. Helicobacter pylori urease, native relative molecular mass approximately 600,000, was purified by agarose gel filtration and ion exchange chromatography. DEAE-purified urease is highly active and has a Km of 0.48 mM for urea. The enzyme has a pI of 5.93 and is active from pH 4.0 to 10.0, with an optimum at pH 8.0. The purified urease contains nickel and is composed of two protein subunits, with relative molecular masses of 66,000 and 31,000. The subunits were separated and purified and the first 30 N-terminal amino acid residues were determined. A remarkably close relationship was found between both H. pylori urease subunits and jack bean (Canavalia ensiformis) urease, the subunit of which is a single 840 amino acid polypeptide. This subunit is also largely identical to the high molecular mass subunits of the ureases of Klebsiella aerogenes and Proteus mirabilis, evidence that these four ureases are derived from a common ancestral protein.
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PMID:Characterization of the Helicobacter pylori urease and purification of its subunits. 185 97


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