Synthesis and activity of Helicobacter pylori urease and catalase at low pH.

Bauerfeind, Peter; Garner, Rachel M.; Dunn, Bruce E.; Mobley, Harry L. T.

doi:10.1136/gut.40.1.25

Cited by 208 publications

(159 citation statements)

References 28 publications

(12 reference statements)

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“…Cells were seeded in 24-wells trays at the density of 10 3 /cm 2 2 days before experiments and then treated with 50 nM VacA preactivated at pH 2.0 in DMEM containing 5 mM NH 4 Cl and various concentrations of phloretin (0-480 µM) at 37°C. After 6 hours, cell vacuolation was quantified using the neutral red uptake assay as described previously (15).…”

Section: Reagentsmentioning

confidence: 99%

The Helicobacter pylori VacA toxin is a urea permease that promotes urea diffusion across epithelia

Tombola¹,

Morbiato²,

Giudice³

et al. 2001

J. Clin. Invest.

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Section: Reagentsmentioning

confidence: 99%

The Helicobacter pylori VacA toxin is a urea permease that promotes urea diffusion across epithelia

Tombola¹,

Morbiato²,

Giudice³

et al. 2001

J. Clin. Invest.

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“…made and is essential for colonization and virulence (Bauerfeind et al 1997;Hu and Mobley 1990;Tsuda et al 1994a;Tsuda et al 1994b), while the hydrogen utilizing hydrogenase provides the bacterium a compact and high energy non-carbon substrate for respiratory based energy generation (Maier et al 1996;Olson and Maier 2002). In addition to these nickel enzymes, H. pylori also possesses a NixA nickel specific permease (Bauerfeind et al 1996), accessory proteins UreIEFGH and HypABCDEF (some of which bind nickel) required for maturation or activation of the apoenzymes for the two nickel enzymes (Benoit et al 2004;Mehta et al 2003a;Olson et al 2001;Voland et al 2003), a nickel dependent regulator, NikR (Contreras et al 2003;van Vliet et al 2002), a recently identified nickel efflux system (CznABC) (Stahler et al 2006) and a histidine-rich heat shock protein, HspA, a GroES homologue Kansau and Labigne 1996).…”

mentioning

confidence: 99%

Nickel-binding and accessory proteins facilitating Ni-enzyme maturation in Helicobacter pylori

2007

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Helicobacter pylori colonizes the human gastric mucosa and this can lead to chronic gastritis, peptic and duodenal ulcers, and even gastric cancers. The bacterium colonizes over one-half of the worlds population. Nickel plays a major role in the bacteriums colonization and persistence attributes as two nickel enzyme sinks obligately contain the metal. Urease accounts for up to 10% of the total cellular protein made and is required for initial colonization processes, and the hydrogen oxidizing hydrogenase provides the bacterium a high-energy substrate yielding low potential electrons for energy generation. A battery of accessory proteins are needed for maturation or activation of each of the apoen-zymes. These include Ni-chaperones and GTPas-es, some of which are unique to each Ni-enzyme and others that are individually required for maturation of both the Ni-enzymes. H. pylori's need for some conventional hydrogenase maturation proteins playing roles in urease maturation may have to do with the poor nickel-sequestering ability of the UreE urease maturation protein compared to other systems. H. pylori also possesses a NixA nickel specific permease, a nickel dependent regulator (NikR), a recently identified nickel efflux system (CznABC), and a histidinerich heat shock protein, HspA. Based on mutant analysis approaches all these proteins have roles in nickel homeostasis, in urease expression, and in host colonization. The His-rich putative nickel storage proteins Hpn and Hpn-like play roles in nickel detoxification and may influence the levels of Ni-activated urease that can be achieved.

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“…The possible reason for the low rate of enteritis in patients with H. pylori infection is that H. pylori can cause pangastritis and reduce gastric acid production [20][21][22][23], thereby raising the pH of the small intestine and protecting against small intestinal mucosal injury.…”

Section: Discussionmentioning

confidence: 99%

Influence of Helicobacter pylori Infection on the Small Intestinal Mucosa

2013

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patients undergoing capsule endoscopy (CE) were tested for anti-H. pylori immunoglobulin G antibody (Hp-IgG) using an enzyme-linked immunosorbent assay (ELISA). None of the patients had been treated for H. pylori infection or diagnosed as having Crohn's disease or any other clinically apparent small intestinal disorders prior to the CE. Results. The overall Hp-IgG-positive rate was 26.3%. The incidence of enteritis, as diagnosed by CE, tended to be lower in the Hp-IgG-positive patients (23.1%) than in the Hp-IgG-negative patients (38.4%) ( = 0.140). When patients receiving aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs), well-known causes of enteritis, were excluded, the incidence of enteritis in the Hp-IgG-positive patients (11.7%) was significantly lower than that in the Hp-IgG-negative patients (43.7%) ( = 0.005). A binomial logistic regression analysis revealed a significant negative relationship between Hp-IgG positivity and the presence of enteritis in patients receiving neither aspirin nor NSAIDs ( = 0.017). Conclusions. Our data indicated that H. pylori positivity was inversely associated with the prevalence of enteritis.

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Synthesis and activity of Helicobacter pylori urease and catalase at low pH.

Cited by 208 publications

References 28 publications

The Helicobacter pylori VacA toxin is a urea permease that promotes urea diffusion across epithelia

The Helicobacter pylori VacA toxin is a urea permease that promotes urea diffusion across epithelia

Nickel-binding and accessory proteins facilitating Ni-enzyme maturation in Helicobacter pylori

Influence of Helicobacter pylori Infection on the Small Intestinal Mucosa

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