Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.1.5 (urease)
 7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with Helicobacter pylori, is one of the most prevalent infections world-wide, where approximately 50% of adults in the developed world and over 90% of inhabitants in the developing world are infected. Chronic infection with H. pylori is the cause of gastritis, peptic ulcer disease and is a risk factor for gastric adenocarcinoma. Recent studies have demonstrated the suitability of an immunization strategy in the prevention and treatment of H. pylori infection, and the potential for management of disease. Mucosal administration of purified recombinant sub-unit proteins of H. pylori, together with a mucosal adjuvant, has identified urease to be highly efficacious in prophylactic and therapeutic animal model studies, and show partial therapeutic activity in humans. Several other antigens are also effective, and the recent sequencing of the H. pylori genome has led to an intensive effort in antigen discovery. Other research has centered on the identification of novel approaches for delivery, and the immunological mechanisms underlying protective immunity. In this review, preclinical data and the results of early-stage clinical trials and directions for future research on Helicobacter vaccines are described.
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PMID:Vaccine development against infection with Helicobacter pylori. 960 46

Infection with Helicobacter hepaticus causes chronic active hepatitis in certain strains of mice and is associated with hepatocellular carcinoma in A/JCr mice. Like the gastric helicobacters, H. pylori and H. mustelae, H. hepaticus possesses a high level of urease activity. However, the H. hepaticus urease structural gene sequences have not been previously determined, and the role of the urease enzyme in colonization and in pathogenesis is not known. PCR was used to amplify a portion of the urease structural genes from H. hepaticus genomic DNA. Amplified DNA fragments were cloned, and the nucleotide sequence was determined. The deduced amino acid sequence of the partial H. hepaticus ureA gene product was found to exhibit 60% identity and 75% similarity to the predicted H. pylori UreA. The deduced amino acid sequence of a partial H. hepaticus ureB gene product exhibited 75% identity and 87% similarity to the predicted H. pylori UreB. Diversity among H. hepaticus isolates was evaluated by means of a restriction fragment length polymorphism (RFLP) assay. The 1.6-kb fragments within the ureAB open reading frames, amplified from 11 independent isolates, were digested with the restriction endonuclease HhaI. Three distinct RFLP patterns were observed. Identical RFLP profiles were noted in sequential isolates of one strain of H. hepaticus during an 18 month in vivo colonization study, suggesting that the urease genes of H. hepaticus are stable. The urease genes among H. hepaticus strains were also well conserved, showing 98.8 to 99% nucleotide sequence identity among three isolates analyzed. These findings indicate that H. hepaticus has urease structural genes which are homologous to those of the gastric Helicobacter species and that these gene sequences can be used in a PCR and RFLP assay for diagnosis of this important murine pathogen.
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PMID:Development of a PCR-restriction fragment length polymorphism assay using the nucleotide sequence of the Helicobacter hepaticus urease structural genes ureAB. 970 72

In Japan, gastric ulcers are often accompanied by marked gastric mucosal atrophy. We evaluated the dual therapy of double-dose lansoprazole and amoxycillin for Helicobacter pylori eradication in Japanese ulcer patients and investigated the effects of intragastric distribution of H. pylori colonization and gastric mucosal atrophy on eradication with this combination therapy. Seventy-six H. pylori-positive ulcer patients received lansoprazole (30 mg) plus amoxycillin (500 mg) twice daily for 2 weeks (LA-60 group), lansoprazole (30 mg once daily) plus amoxycillin (500 mg twice daily) for 2 weeks (LA-30 group) or lansoprazole (30 mg once daily) for 6 or 8 weeks (LPZ group). Infection was evaluated by light microscopy, culture and biopsy urease tests. Helicobacter pylori colonization was classified as localized to the corpus (localized type) or involving the antrum and corpus (whole type). Fundic mucosal atrophy was graded according to endoscopic and histological features. Eradication was achieved in 67.6% in the LA-60 group, 31.6% in the LA-30 group, and 0% in the LPZ group, and moderate or severe histological gastritis was improved in the LA-60 group. Eradication was better in localized-type colonization (92%) than whole-type (56%), and better with fundic mucosal atrophy (84%) than without, but poor in both whole-type colonization and scanty mucosal atrophy (47%). The LA-60 therapy achieves better eradication in Japanese ulcer patients with localized H. pylori colonization and/or gastric mucosal atrophy, which are likely to be important predictors for the successful eradication with dual therapy.
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PMID:Factors influencing Helicobacter pylori eradication with 2 week combination therapy of lansoprazole and amoxycillin: intragastric distribution of colonization and gastric mucosal atrophy. 971 25

Experimental Helicobacter pylori infection was studied in Mongolian gerbils with fresh human isolates that carry or do not carry cagA (cagA-positive or cagA-negative, respectively), multiply passaged laboratory strains, wild-type strain G1.1, or isogenic ureA, cagA, or vacA mutants of G1.1. Animals were sacrificed 1 to 32 weeks after challenge, the stomach was removed from each animal for quantitative culture, urease test, and histologic testing, and blood was collected for antibody determinations. No colonization occurred after >/=20 in vitro passages of wild-type strain G1.1 or with the ureA mutant of G1.1. In contrast, infection occurred in animals challenged with wild-type G1.1 (99 of 101 animals) or the cagA (25 of 25) or vacA (25 of 29) mutant of G1.1. Infection with G1.1 persisted for at least 8 months. All 15 animals challenged with any of three fresh human cagA-positive isolates became infected, in contrast to only 6 (23%) of 26 animals challenged with one of four fresh human cagA-negative isolates (P < 0.001). Similar to infection in humans, H. pylori colonization of gerbils induced gastric inflammation and a systemic antibody response to H. pylori antigens. These data confirm the utility of gerbils as an animal model of H. pylori infection and indicate the importance of bacterial strain characteristics for successful infection.
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PMID:Experimental infection of Mongolian gerbils with wild-type and mutant Helicobacter pylori strains. 974 90

Two types of canine struvite uroliths have been recognized: infection-induced struvite is the most common type; sterile struvite is uncommonly recognized. Infection-induced struvite is most commonly associated with urease-producing staphylococcal UTI. For dogs that qualify, medical dissolution is an effective method of treatment. Medical dissolution protocols encompass: (1) eradication or control of UTI; (2) use of calculolytic diets; and (3) administration of urease inhibitors to patients with persistent UTI caused by urease-producing microbes.
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PMID:Medical dissolution and prevention of canine struvite urolithiasis. Twenty years of experience. 1002 53

Infection by Helicobacter pylori (HP) occurs all over the world and is related to the socio-economic development of the subject's country of residence and age. Various strains of HP can be identified on the basis of the microbiological characteristics of the bacterium and, in particular, or its antigenic profile, while the virulence factors are responsible for the damage that HP can cause. The virulence factors include components (flagellum and adhesin) and substances produced by bacterium (enzymes and cytotoxins), the most important among which are urease and the cytotoxins, CagA and VacA. It is the association of these virulence factors that is responsible for the different pathologies to which HP-positive subjects are prone. The link between HP and gastritis, peptic ulcer and gastric cancers (adenocarcinoma and lymphoma) is now proven. Whether there is a link between HP and RAP in young children is still a matter for debate; some Authors claim that there is, while others refute it.
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PMID:[Helicobacter pylori. I. Morphology, biochemistry, antigenic profile and correlated diseases]. 1006 80

This study evaluated the sensitivity of serological and direct methods for the diagnosis of Helicobacter pylori infection in 127 patients with gastric carcinoma and in 127 controls without this disease, matched for age and sex. Antral and oxyntic mucosal specimens were obtained from all patients, at operation in patients with gastric carcinoma and at endoscopy from controls. The urease test, microscopy of stained smears and culture for H. pylori were performed on all specimens. Sera from all patients were tested for antibodies to H. pylori by a highly sensitive and specific IgG-ELISA. Culture, urease test, stained smear and ELISA were significantly less sensitive in the patients with gastric carcinoma than in control subjects. However, the combination of several methods improved the diagnosis of H. pylori infection in the gastric carcinoma group. Infection was significantly more frequent in the gastric carcinoma patients than in the controls. H. pylori infection was associated with an increased risk of developing gastric carcinoma.
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PMID:Serological and direct diagnosis of Helicobacter pylori in gastric carcinoma: a case-control study. 1022 48

Forty-seven fusidic acid- and methicillin-resistant Staphylococcus aureus isolates from clinical samples in four hospitals in Kuwait were studied for their relatedness by biotyping and pulsed-field gel electrophoresis (PFGE) and for the genetic location of their resistance determinants. Forty-four isolates were resistant to gentamicin, kanamycin and neomycin. Forty-one isolates were resistant to erythromycin and trimethoprim, 10 were resistant to chloramphenicol and four were resistant to ciprofloxacin. They contained two or three plasmids of c. 28, 2.8 and 1.8 kb. Genetic studies demonstrated that resistance to cadmium, propamidine isethionate and ethidium bromide were linked and were carried on the c. 28-kb plasmid. Chloramphenicol resistance was encoded by the 2.8-kb plasmid in resistant isolates. No resistance was associated with the 1.8-kb plasmid and this was considered to be a cryptic plasmid. Resistance to fusidic acid, methicillin, benzylpenicillin, gentamicin, kanamycin, neomycin, tetracycline, trimethoprim, erythromycin and ciprofloxacin were located on the chromosome. All the isolates produced urease, but varied in the production of haemolysins, pigments, lipase and lecithinase and were classified into nine biotypes. In contrast, PFGE divided the isolates into two major patterns with one PFGE type constituting the majority of isolates in all four hospitals. The presence of the dominant PFGE pattern in all four hospitals suggests that it is an epidemic MRSA clone with the capacity to spread. Infection control measures should be directed towards restricting the further spread of this clone.
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PMID:Characterisation of methicillin-resistant Staphylococcus aureus from Kuwait hospitals with high-level fusidic acid resistance. 1079 54

Infection with Helicobacter pylori induces humoral immune responses against various antigens of the bacterium. Heat shock proteins (hsps) are immunodominant antigens in various diseases including H. pylori infection. In the present study, we measured the anti-hsp antibody titers in 42 patients with H. pylori-infected peptic ulcers during a bacterial eradication study. The patients were treated with a proton pump inhibitor and antimicrobial agents to eradicate the organism. Their sera were obtained at pretreatment and at 1 month and 6 months after the eradication therapy. The titers of immunoglobulin G antibodies to the H. pylori hsp, whole-cell lysate, and urease (30-kDa subunit) antigens in serum were measured by a capture enzyme-linked immunosorbent assay. The levels of H. pylori hsp60 antibodies in sera collected 1 month after treatment had declined significantly, even when changes in the titers of antibodies to whole-cell and urease antigens were not apparent. These results suggest that measurement of antibodies to H. pylori hsp60 in serum is useful for the early monitoring of the effectiveness of eradication therapy.
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PMID:Antibody to heat shock protein can be used for early serological monitoring of Helicobacter pylori eradication treatment. 1088 54

Infection by Helicobacter pylori leads to injury of the gastric epithelium and a cellular infiltrate that includes CD4+ T cells. H. pylori binds to class II MHC molecules on gastric epithelial cells and induces their apoptosis. Because urease is an abundant protein expressed by H. pylori, we examined whether it had the ability to bind class II MHC and induce apoptosis in class II MHC-bearing cells. Flow cytometry revealed the binding of PE-conjugated urease to class II MHC+ gastric epithelial cell lines. The binding of urease to human gastric epithelial cells was reduced by anti-class II MHC Abs and by staphylococcal enterotoxin B. The binding of urease to class II MHC was confirmed when urease bound to HLA-DR1-transfected COS-1 (1D12) cells but not to untransfected COS-1 cells. Urease also bound to a panel of B cell lines expressing various class II MHC alleles. Recombinant urease induced apoptosis in gastric epithelial cells that express class II MHC molecules, but not in class II MHC- cells. Also, Fab from anti-class II MHC and not from isotype control Abs blocked the induction of apoptosis by urease in a concentration-dependent manner. The adhesin properties of urease might point to a novel and important role of H. pylori urease in the pathogenesis of H. pylori infection.
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PMID:Helicobacter pylori urease binds to class II MHC on gastric epithelial cells and induces their apoptosis. 1092 73


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