Literature DB >> 2379775

Urea protects Helicobacter (Campylobacter) pylori from the bactericidal effect of acid.

B J Marshall1, L J Barrett, C Prakash, R W McCallum, R L Guerrant.   

Abstract

Colonization of the stomach with Helicobacter (Campylobacter) pylori is common in patients with duodenal ulcer disease, which is known for its high acid secretion. Although the bacterium is usually isolated by culture of a gastric biopsy specimen, viable organisms may sometimes be found in the acidic gastric juice. It was postulated that urease, by generating ammonia, protected H. pylori from acid. To test this hypothesis, the pH susceptibility of H. pylori, Proteus mirabilis, and the urease-negative Campylobacter jejuni was examined in the presence and absence of urea. It was found that without urea the three bacteria were all highly susceptible to acid. In striking contrast, the addition of 5 mmol/L of urea completely protected H. pylori but not P. mirabilis or C. jejuni from pH values as low as 1.5. Furthermore, the protective effect of urea on H. pylori was found with urea concentrations as low as 0.05 mmol/L. It is concluded that the high urease activity of H. pylori enables it to survive in gastric acid.

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Year:  1990        PMID: 2379775     DOI: 10.1016/0016-5085(90)90957-3

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  113 in total

1.  Significance of blood urea: gastric ammonia gradient for H. pylori detection in childhood.

Authors:  Alexander A Nijevitch; Valentine V Loguinovskaya
Journal:  Dig Dis Sci       Date:  2002-01       Impact factor: 3.199

2.  Identification of virulence genes of Helicobacter pylori by random insertion mutagenesis.

Authors:  J J Bijlsma; C M Vandenbroucke-Grauls; S H Phadnis; J G Kusters
Journal:  Infect Immun       Date:  1999-05       Impact factor: 3.441

Review 3.  Role of Helicobacter pylori in duodenal ulcer.

Authors:  E A Rauws
Journal:  Drugs       Date:  1992-12       Impact factor: 9.546

4.  The urease enzyme of Helicobacter pylori does not function as an adhesin.

Authors:  M Clyne; B Drumm
Journal:  Infect Immun       Date:  1996-07       Impact factor: 3.441

5.  Acidic pH changes receptor binding specificity of Helicobacter pylori: a binary adhesion model in which surface heat shock (stress) proteins mediate sulfatide recognition in gastric colonization.

Authors:  M Huesca; S Borgia; P Hoffman; C A Lingwood
Journal:  Infect Immun       Date:  1996-07       Impact factor: 3.441

6.  Helicobacter pylori survival in gastric mucosa by generation of a pH gradient.

Authors:  G Chen; R L Fournier; S Varanasi; P A Mahama-Relue
Journal:  Biophys J       Date:  1997-08       Impact factor: 4.033

7.  Ammonia, hydrogen peroxide, and monochloramine retard gastric epithelial restoration in rabbit cultured cell model.

Authors:  K Sato; S Watanabe; T Yoshizawa; M Hirose; T Murai; N Sato
Journal:  Dig Dis Sci       Date:  1999-12       Impact factor: 3.199

8.  A bifunctional urease enhances survival of pathogenic Yersinia enterocolitica and Morganella morganii at low pH.

Authors:  G M Young; D Amid; V L Miller
Journal:  J Bacteriol       Date:  1996-11       Impact factor: 3.490

9.  Helicobacter mustelae-induced gastritis and elevated gastric pH in the ferret (Mustela putorius furo).

Authors:  J G Fox; G Otto; N S Taylor; W Rosenblad; J C Murphy
Journal:  Infect Immun       Date:  1991-06       Impact factor: 3.441

10.  Helicobacter pylori in vivo causes structural changes in the adherent gastric mucus layer but barrier thickness is not compromised.

Authors:  J L Newton; N Jordan; L Oliver; V Strugala; J Pearson; O F James; A Allen
Journal:  Gut       Date:  1998-10       Impact factor: 23.059

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