[PDF] Characteristics of Helicobacter pylori variants selected for urease deficiency | Semantic Scholar (2024)

Urease activity has recently been shown to be an important virulence determinant for Helicobacter pylori, allowing it to survive the low pH of the stomach during colonization and to be inhibited in a competitive manner by flurofamide.

It is concluded that cytoplasmic urease activity alone is not sufficient to allow survival of H. pylori in an acid environment and that the activity of surface-localized ure enzyme is essential for resistance ofH.

The aim of this work was to study the significance of the urease enzyme in promoting Helicobacter pylori survival in various environments and to suggest that the acid environment of the stomach may be crucial for H. pyloris survival in the presence of urea.

The MIU test that showed high sensitivity and specificity, and thus could be further developed as an alternative diagnostic method for H. pylori infection.

Surface-bound urease is too low to contribute to acid resistance and is part of the gastric colonization strategy of the organism.

Results to date have shown that in addition to PBP1, changes in outer membrane permeability are required to get high level amoxicillin resistance, and in order to track both the evolution of resistance as well as identify other possible novel resistance mechanisms, whole genome sequencing of the most resistant isolate was used.

Results indicated that H. pylori urease is essential for colonizing the nude mouse stomach, and that gastritis was found in the CPY3401-challenged stomachs, from which bacteria indistinguishable from CPy3401 were recovered.

A procedure that permits the cultivation of a gram-positive coccoid species from biopsy material obtained from the antrum of the stomachs of patients with gastric disorders is devised, which would be expected to proliferate outside of the human host as well as in the gastric mucosa.

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The results suggest that prominent urease activity is essential for colonization by H. pylori.

The urea of H. pylori probably causes this vacuolization of tissue culture cells by H.pylori, and it was found that the final pH was 7.6, indicating that vacUolization was not due to change of pH.

Data indicate that antigenic 128- and 82-kDa proteins are present in H. pylori broth culture supernatants with vacuolizing activity and that serologic responses to the 128-k da protein are more prevalent among H.pylori-infected persons with duodenal ulceration than among infected persons without peptic ulcerations.

It was concluded that C. pylori can produce a factor that alters cultured cells in vitro that is neutralisable by specific antisera to broth-culture filtrates or to sonicated bacteria but not by antisersa to other bacterial preparations.

Observations indicate that the vacuolating activity in H. pylori supernatants is not mediated solely by urease activity but that it may be potentiated by Urease-mediated ammonia production.

The bacteria had most of the characteristics of Campylobacter spp.

Findings indicate that the suicidal destruction of the bacterium may be explained by intracellular accumulation of ammonia due to production in excess of the rate of excretion.

Evidence from human volunteer studies, therapeutic trials with antimicrobial agents, and experiments with animal models indicates that H. pylori plays an etiologic role in the pathogenesis of type B gastritis.

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