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Updated: Jul 11, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
09:05

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

The pepsinogen releasing effect of Helicobacter pylori lipopolysaccharide

G O Young1, S Brown, N Stemmet

  • 1GI Clinic and Department of Medicine, University of CapeTown, South Africa.

Helicobacter
|April 10, 2002
PubMed
Abstract

Insights

Helicobacter pylori lipopolysaccharide (LPS) stimulates pepsinogen release, an innate property of all cagA+ strains. The molecule's structure and side-chains, partly driven by lipid A, are crucial for this effect.

Area of Science:

  • Gastroenterology
  • Microbiology
  • Immunology

Background:

  • Helicobacter pylori lipopolysaccharide (LPS) influences pepsinogen release via a non-toxic pathway.
  • The study investigated if this effect is strain-specific and linked to clinical status.

Purpose of the Study:

  • To determine if H. pylori LPS elicits pepsinogen release.
  • To assess if this effect is specific to H. pylori and related to strain characteristics.

Main Methods:

  • LPS from 11 H. pylori strains and 4 other bacteria were isolated.
  • Pepsinogen release was measured in guinea pig gastric mucosa using Ussing chambers.
  • The impact of LPS structural modifications (Polymyxin B, dephosphorylation) was assessed.

Main Results:

  • H. pylori LPS dose-dependently stimulated pepsinogen release.
  • LPS from other Helicobacter or Campylobacter species showed no effect.
  • Significant variations in pepsinogen release efficacy were observed among H. pylori strains, linked to LPS structure and lipid A.

Conclusions:

  • Pepsinogen release is an intrinsic characteristic of all cagA+ H. pylori LPS.
  • LPS structure and side-chain composition are critical for this response.
  • The mechanism appears to be partially driven by lipid A.

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