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  • 1
    Electronic Resource
    Electronic Resource
    Helicobacter pylori lipopolysaccharide stimulates gastric mucosal pepsinogen secretion (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 6 (1992), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of Helicobacter pylori lipopolysaccharide on guinea pig gastric mucosal pepsinogen secretion has been examined using an Ussing chamber technique. Luminal addition of H. pylori lipopolysaccharide resulted in a fifty-fold stimulation of pepsinogen secretion compared to a twelve-fold increase with E. coil lipopolysaccharide. Electron microscopy showed marked degranulation of zymogen granules but no evidence of chief cell disruption.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.1992.tb00260.x
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  • 2
    Electronic Resource
    Electronic Resource
    The Pepsinogen Releasing Effect of Helicobacter pylori Lipopolysaccharide (2002)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 7 (2002), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Helicobacter pylori lipopolysaccharide (LPS) affects pepsinogen release by a nontoxic mechanism. We hypothesized that this effect was characteristic of the organism and related to the clinical status of the strain.Materials and methods. LPS was isolated from 11 H. pylori strains whose pathogenic profile was known and four other nongastric bacteria. The effects of luminal LPS on guinea pig gastric mucosal pepsinogen release was evaluated using the Ussing chamber technique. CCK-8 (10−9M) was used as a positive control.Results. H. pylori LPS dose-dependently stimulated pepsinogen release with a maximal stimulation at 250 µg/ml (~4500%; p 〈 .001 vs. control). LPS from other Helicobacter or Campylobacter species had no effect on pepsinogen release. ANOVA demonstrated significant differences in the efficacies of pepsinogen release between the 11 clinical H. pylori strains (p 〈 .0001) despite the fact that they were all cagA+ and 90% had the cytotoxic vacA subtype s1. Physical and chemical disruption of the LPS suggested that both the structure and the carbohydrate composition of this molecule may play a critical role in pepsinogen release. Polymyxin B partly (p 〈 .03) inhibited and dephosphorylation completely inhibited (p = .0002) LPS-stimulated pepsinogen release.Conclusion. Pepsinogen release is an innate property of all cagA+H. pylori LPS. The structure of the molecule and composition of side-chains are important in this response which appears to be partially lipid A driven.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.2002.00053.x
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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