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 membrane-like flagellar sheath of Helicobacter pylori is of unknown function and little is known of its composition. A murine monoclonal antibody to H. pylori, designated GF6, which reacts by immunoblot with a polypeptide with an apparent molecular mass of 29 kDa was shown by immunogold-electron microscopy to label specifically the flagellar sheath structure. The antigen was detected by immunoblot using the monoclonal antibody in all 11 strains, of diverse geographic origin, so far tested. The antibody also reacted weakly with polypeptides with apparent molecular masses of 65 kDa in Vibrio cholerae and Vibrio parahaemolyticus. The antigen was shown by one- and two-dimensional electrophoretic analysis and immunoblotting to be distinct from the abundant urease subunit UreA, of similar molecular mass. Identification of this flagellar sheath polypeptide will facilitate investigation of the structure and function of the flagellar sheath of this important gastric pathogen.
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PMID:Identification of a 29 kDa flagellar sheath protein in Helicobacter pylori using a murine monoclonal antibody. 771 97

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

Urease is an important virulence factor for gastric Helicobacter spp. To elucidate the efficacy of individual urease subunits to act as mucosal immunogens, the genes encoding the respective urease subunits (UreA and UreB) of Helicobacter pylori and Helicobacter felis were cloned in an expression vector (pMAL) and expressed in Escherichia coli cells as translational fusion proteins. The recombinant UreA and UreB proteins were purified by affinity and anion-exchange chromatography techniques and had predicted molecular masses of approximately 68 and 103 kDa, respectively. Western blotting (immunoblotting) studies indicated that the urease components of the fusion proteins were strongly immunogenic and were specifically recognized by polyclonal rabbit anti-Helicobacter sp. sera. The fusion proteins (50 micrograms) were used, in combination with a mucosal adjuvant (cholera toxin), to orogastrically immunize mice against H. felis infection. Gastric tissues from H. felis-challenged mice were assessed by the biopsy urease test and by histology. In mice immunized with recombinant H. felis UreB, 60% of animals (n = 7) were histologically negative for H. felis bacteria after challenge at 17 weeks. This compared with 25% (n = 8) for mice immunized with the heterologous H. pylori UreB antigen. Neither the homologous nor the heterologous UreA subunit elicited protective responses against H. felis infection in mice. The study demonstrated that a recombinant subunit antigen could induce an immunoprotective response against gastric Helicobacter infection.
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PMID:Recombinant antigens prepared from the urease subunits of Helicobacter spp.: evidence of protection in a mouse model of gastric infection. 792 78

The common mucosal immune system was stimulated by oral immunisation with jack bean urease and the adjuvant cholera toxin. A high level of local antibody and serum antibody was induced in mice following hyperimmunisation with this combination. No cross-reacting antibody was found against either Helicobacter pylori or Helicobacter felis. No protection was observed against oral challenge of immunised mice with living H. felis thus disproving the interesting hypothesis of Pallen and Clayton that plant urease might induce a protective immunity against helicobacter infection.
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PMID:Lack of protection against gastric Helicobacter infection following immunisation with jack bean urease: the rejection of a novel hypothesis. 818 96

Attenuated Vibrio cholerae O1 vaccine strains lacking the gene encoding the A subunit of cholera toxin have proven efficacious in preventing experimental cholera. As these strains move from closed, contained testing environments to large-scale field trials, a readily assayable phenotypic trait to distinguish a vaccine strain from wild-type V. cholerae O1 is desirable. We have constructed three derivatives of the attenuated V. cholerae strain CVD 103 which carry a mercury resistance or urease marker in the hlyA gene. CVD 103-HgR was constructed using a protracted marker-exchange procedure; this strain was found to have somewhat lowered colonisation efficiency in infant mice in comparison to its parent strain, CVD 103. The insertion of the resistance marker was repeated using a suicide vector system; CVD 103-HgR2 was found to colonise infant mice as efficiently as CVD 103. Strain CVD 103-UR, in which sequences encoding urease were inserted using a suicide vector, also colonised infant mice as well as CVD 103. The genetically marked strains CVD 103-HgR, CVD 103-HgR2 and CVD 103-UR form the basis for a generation of defined oral vaccines that may give single-dose, long-lasting protection to populations at risk from cholera.
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PMID:Construction of genetically marked Vibrio cholerae O1 vaccine strains. 835 76

Following the demonstration of Helicobacter pylori as a major gastroduodenal pathogen there was a need to develop animal models in order to investigate mechanisms of pathogenesis and to be able to test new treatment strategies. Helicobacter pylori will only colonize a limited number of hosts including non-human primates, germ-free or barrier raised piglets, germ-free dogs and recently laboratory raised cats. Although these models have proved useful there is a need for more convenient small animal models. The ferret infected with its natural gastric organism, Helicobacter mustelae, is the only other animal to show peptic ulceration and has been successfully used to investigate gastritis and antimicrobial agents. The other commonly used animal model is the laboratory mouse or rat infected with either Helicobacter felis or Helicobacter heilmannii, bacteria that normally colonize cat or dog gastric mucosae. Active/chronic gastritis, gastric atrophy, and lymphoma-like lesions have been shown to develop in H. felis infected mice. The most recent and exciting use of an animal model has been the use of the H. felis mouse model in the development of human vaccines against H. pylori. Mice can be protected against infection with large doses of viable H. felis by oral immunization using sonicates of H. felis or H. pylori or recombinant H. pylori urease together with cholera toxin or cholera toxin-B subunit as the mucosal adjuvant. More importantly it has been shown that immunization of already infected animals results in eradication of infection. This raises the intriguing possibility that therapeutic immunization might be a viable option in the management of Helicobacter-associated disease. If immunization as a therapy of peptic ulcers was combined with short-term acid suppression, the possibility of reinfection may also be eliminated. In those countries where H. pylori infection rates are very high and infection occurs at an early age, large scale oral immunization of sections of the community would not only protect the young from the deleterious consequences of long-term H. pylori infection but could also cure existing disease.
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PMID:Animal models and vaccine development. 856 56

The initial steps have been taken towards the development of a vaccine against the human gastroduodenal pathogen, Helicobacter pylori. Proof of principle was achieved when mice were protected against challenge with living Helicobacter felis, a close relative of the human pathogen, following oral immunization with H. felis sonicate and the mucosal adjuvant, cholera toxin. Similar results with H. pylori antigen have allowed development of possible human vaccines. Recombinant urease protein has been proposed as a major vaccine candidate, together with the heat-labile toxin of Escherichia coli as the adjuvant. Probably the most significant finding in the early vaccine studies was that immunization of already infected mice resulted in a cure of Helicobacter infection. The possibility of a therapeutic vaccine makes commercial development more attractive, as large populations could be immunized without the potential for development of drug-resistant strains that currently restricts widespread antibiotic use. For advanced societies with powerful economies yet a high prevalence of H. pylori, such as Japan, vaccine development should become a high national health priority.
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PMID:Vaccination against Helicobacter pylori. 895 25

Intranasal (i.n.) delivery of antigen can be highly effective for generating circulating and secretory antibody responses. Mice were immunized i.n. with two antigens, human IgA, and Helicobacter pylori urease in the presence or absence of mucosal adjuvant. To restrict antigen delivery to the upper airways, protein solutions were administered in a small volume without anesthesia. Repeated daily i.n. administration of antigen without adjuvant elicited high levels of specific IgG in serum and IgA in serum, saliva, and feces. Once weekly i.n. immunization with co-administration of cholera toxin or Escherichia coli heat-labile toxin as adjuvant elicited somewhat lower levels of antibody to urease. When challenged with Helicobacter felis, only mice immunized with urease in the presence of adjuvant were protected against gastric infection.
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PMID:Novel intranasal immunization techniques for antibody induction and protection of mice against gastric Helicobacter felis infection. 914 Dec 7

The outer surface protein A (OspA) lipoprotein of Borrelia burgdorferi, like cholera toxin and the heat-labile enterotoxin of Escherichia coli, induces pro-inflammatory cytokines. This suggested that, like those toxins, OspA might be a mucosal immunogen and adjuvant. OspA, administered intranasally (i.n.) or intragastrically, induced strong serum IgG and salivary gland IgA responses. The serum IgG isotypes were indicative of a mixed T helper 1 and T helper 2 response, the latter being more pronounced. The N-terminal tripalmitoyl-S-glyceryl-cysteine (Pam3Cys) lipid moiety was absolutely required. OspA strongly enhanced the serum IgG and salivary gland IgA responses to jack bean urease co-administered by the i.n. route. OspA also enhanced the response to tetanus toxoid and induced limited protection against challenge. A synthetic lipopeptide also adjuvanted the response to urease by the i.n. route, but was ca 500-fold less potent on a molar basis than OspA. These results suggest that OspA or other lipoproteins may be useful in mucosal vaccines.
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PMID:OspA lipoprotein of Borrelia burgdorferi is a mucosal immunogen and adjuvant. 926 45

In analogy with Vibrio cholerae and other toxigenic enteropathogens such as Yersinia enterocolitica it seems most likely today that H. pylori by specific surface proteins binds to epithelial cell receptors (Table 1) allowing the pathogen to deliver urease, vacuolating toxin and other toxic metabolites to cause tissue damage and inflammation (1-3). H. pylori as well as animal gastric pathogens as H. mustelae and H. felis have developed an efficient flagellar apparatus allowing rapid and efficient penetration of the gastric mucus layer (3). Most interestingly, flagellae seems to be synthesized in the late stage of growth before the switch of spiral-shaped organisms to coccoidal forms in a liquid medium.
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PMID:Biochemical aspects of H. pylori adhesion. 937 15


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