title: The pepsinogen releasing effect of Helicobacter pylori lipopolysaccharide.
abstract: 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.
  
  
  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(-9)M) was used as a positive control.
  
  
  RESULTS
  H. pylori LPS dose-dependently stimulated pepsinogen release with a maximal stimulation at 250 microg/ml (approximately 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: GI Clinic and Department of Medicine, University of CapeTown, South Africa.
authors.forename: G O
authors.initials: GO
authors.lastname: Young
authors.forename: S
authors.initials: S
authors.lastname: Brown
authors.forename: N
authors.initials: N
authors.lastname: Stemmet
authors.forename: A J
authors.initials: AJ
authors.lastname: Lastovica
authors.forename: I N
authors.initials: IN
authors.lastname: Marks
authors.forename: I M
authors.initials: IM
authors.lastname: Modlin
authors.forename: M
authors.initials: M
authors.lastname: Kidd
mesh_terms: D000328:Adult; D000818:Animals; D004381:Duodenal Ulcer / Q000382:microbiology; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D006168:Guinea Pigs; D016481:Helicobacter Infections / Q000382:microbiology; D016480:Helicobacter pylori / Q000378:metabolism* / Q000472:pathogenicity; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D010435:Pepsinogens / Q000378:metabolism*; D014774:Virulence
chemical_list: D008070:Lipopolysaccharides; D010435:Pepsinogens