IV. <i>Helicobacter pylori</i> and peptic ulceration: Histopathological aspects

Dixon, M. F.

doi:10.1111/j.1440-1746.1991.tb01451.x

Cited by 200 publications

(86 citation statements)

References 58 publications

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“…H. pylori causes gastritis and is associated with the development of gastric and duodenal ulceration (6,15,34,35), mucosa-associated lymphoid tissue lymphoma, and gastric cancer (7,21). In order to withstand the acidic stomach environment, H. pylori synthesizes large amounts of the nickel-dependent enzyme urease (3,27), an essential virulence and colonization factor for this organism (18,19,49).…”

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Nickel Represses the Synthesis of the Nickel Permease NixA ofHelicobacter pylori

Wolfram¹,

Haas

Bauerfeind³

2006

J Bacteriol

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Nickel acquisition is necessary for urease activity, a major virulence factor of the human gastric pathogen Helicobacter pylori. NixA was identified as a specific nickel uptake system in this organism. Addition of small amounts of nickel to media strongly stimulates urea hydrolysis. On the other hand, high nickel concentrations are deleterious to cell growth. As a possible protective reaction, nickel uptake seems to be reduced in H. pylori grown in nickel-rich media. These observations led to investigations of regulation of the expression of the nickel permease NixA. We found that increasing the nickel concentration in media reduced the amount of NixA. In order to address the question of whether this phenomenon was subject to transcriptional or translational regulation, we quantified nixA mRNA from H. pylori by real-time PCR. The amount of nixA mRNA was gradually reduced five-to sevenfold in a time-and concentration-dependent manner. Repression could be measured as soon as 5 min after nickel addition, and the maximum repression occurred after 20 to 30 min. The maximum repression was obtained with an external nickel concentration of 100 M. The observed nickel repression of NixA was dependent on nikR encoding the nickel-responsive regulatory protein NikR. In conclusion, we demonstrated that synthesis of the NixA nickel permease of H. pylori shows nickel-responsive regulation mediated by NikR to maintain the balance between effective nickel acquisition and a toxic overload.

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Nickel Represses the Synthesis of the Nickel Permease NixA ofHelicobacter pylori

Wolfram¹,

Haas

Bauerfeind³

2006

J Bacteriol

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“…Infection with H. pylori is the most important cause of both peptic ulcer disease and gastric adenocarcinoma, especially involving the distal stomach (2,3,8). Almost all patients with duodenal ulcers and 80 to 90% of gastric ulcer patients are infected with H. pylori in the stomach (32).…”

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Effects of Oral Vaccination and Immunomodulation by Cholera Toxin on ExperimentalHelicobacter pyloriInfection, Reinfection, and Gastritis

2002

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Therapeutic vaccination is an attractive strategy to control infection and disease caused by Helicobacter pylori. In mice infected with H. pylori we have studied the protective effect of oral immunization with an H. pylori lysate preparation given together with the mucosal adjuvant cholera toxin (CT), both against the initial infection and against a later reinfection challenge. We have also examined the effects of treatment with the CT adjuvant alone on H. pylori infection and reinfection. Specific immunization with lysate was found to result in a sixfold reduction of the extent (bacterial load) of the primary infection and also to provide similar levels of protection against reinfection. However, these effects were associated with severe postimmunization gastritis. In contrast, oral treatment with CT alone at the time of initial infection, while unable to suppress the initial infection, gave rise to a 20-fold reduction in bacterial load upon reinfection without causing any associated gastric inflammation. Both the infected animals that were specifically immunized and those that were treated with CT only displayed increased in vitro proliferative responses of mononuclear cells to H. pylori antigens. Antibody levels in response to H. pylori were on the other hand only marginally increased after treatment with CT, whereas they were markedly elevated after immunization with lysate plus CT, with a rise in both (Th2-driven) immunoglobulin G1 (IgG1) and, especially, (Th1-driven) IgG2a antibodies. The results illustrate the complex balance between protection and harmful inflammation after postinfection vaccination against H. pylori as studied in a mouse model.

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“…It converts urea to ammonia and carbamate, the latter decomposing spontaneously to carbon dioxide and ammonia. The released ammonia has been postulated to allow the survival of H. pylori and its colonization of the low-pH environment of the gastric mucosa, which causes Type B gastritis as well as gastric and duodenal ulceration (1,4,19,23,24). Persistent infection is strongly associated with the development of gastric carcinoma and MALT lymphoma (10,29,34).…”

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Conserved Low-Affinity Nickel-Binding Amino Acids Are Essential for the Function of the Nickel Permease NixA of Helicobacter pylori

Wolfram

Bauerfeind

2002

J Bacteriol

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The transition metal nickel is an essential trace element of at least five biological processes (14, 31): (i) hydrolysis of urea, (ii) oxidation and evolution of molecular hydrogen, (iii) carbon monoxide dehydrogenase-mediated acetate metabolism under anaerobic conditions, (iv) reduction of methyl coenzyme M to methane, and (v) detoxification of superoxide anion radicals. Uptake of nickel is a prerequisite for those organisms which catalyze nickel-dependent reactions. Ni 2ϩ -the most prevalent form-is taken up by nonspecific Mg 2ϩ transport systems and high-affinity systems specific for the transport of nickel (see reference 8 for a review).In general, two types of nickel-specific uptake systems have been identified so far: (i) the multiple-component ATP binding cassette system called Nik, which was thought for a long time to be unique to Escherichia coli (39), until homologous systems were identified and characterized in Brucella suis (17) and Vibrio parahaemolyticus (28); and (ii) the nickel-cobalt transporter family, comprising homologous single polypeptides in a variety of microorganisms (8, 32)-Helicobacter pylori (25), Ralstonia eutropha (7), Bradyrhizobium japonicum (11), Rhodococcus rhodochrous (18), and the thermophilic Bacillus species strain TB-90 (21)-which have all been characterized biochemically, or at least physiologically. During database searches, related sequences have been identified in the genomes of Mycobacterium tuberculosis and Mycobacterium avium; Salmonella enterica serovar Paratyphi, Salmonella enterica serovar Typhi, and Salmonella enterica serovar Typhimurium; Staphylococcus aureus; Yersinia pestis; and the fission yeast Schizosaccharomyces pombe (8).Members of the second family share two recognition sequences within their common topology of eight transmembrane helices (TMs): NH 2 -Arg/Lys-His-Ala-Xaa-Asp-Ala-Asp-HisIle/Leu-COOH in TM II and NH 2 -Gly-(Xaa) 2 -Phe-(Xaa) 2 -Gly-His-Ser/Thr-Ser/Thr-Val/Ile-Val-COOH in TM III (32). Besides these two conserved motifs, 48 other conserved amino acids scattered through the protein could be detected after sequence alignment. Recently, two other motifs have been proposed (9): NH 2 -Leu-Gly-Xaa-Asp/Glu-Thr-Ala/Ser-Thr/ Ser-Glu-COOH in TM V and NH 2 -Gly-Met-(Xaa) 3 -Asp-Thr/ Ser-Xaa-Asp-COOH in TM VI.The high-affinity nickel transport protein NixA of the human pathogen H. pylori was discovered when a gene bank clone of strain ATCC 43504 was found to enhance the coexpressed urease activity in E. coli (25). The urease-an important virulence factor of H. pylori-is a major sink of nickel in this organism, representing up to 6% of the soluble cell protein (16). It converts urea to ammonia and carbamate, the latter decomposing spontaneously to carbon dioxide and ammonia. The released ammonia has been postulated to allow the survival of H. pylori and its colonization of the low-pH environment of the gastric mucosa, which causes Type B gastritis as well as gastric and duodenal ulceration (1,4,19,23,24). Persistent infection is strongly associated with...

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IV. Helicobacter pylori and peptic ulceration: Histopathological aspects

Cited by 200 publications

References 58 publications

Nickel Represses the Synthesis of the Nickel Permease NixA ofHelicobacter pylori

Nickel Represses the Synthesis of the Nickel Permease NixA ofHelicobacter pylori

Effects of Oral Vaccination and Immunomodulation by Cholera Toxin on ExperimentalHelicobacter pyloriInfection, Reinfection, and Gastritis

Conserved Low-Affinity Nickel-Binding Amino Acids Are Essential for the Function of the Nickel Permease NixA of Helicobacter pylori

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