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

Dynamics of the Cag-type IV secretion system of Helicobacter pylori as studied by bacterial co-infections

Luisa F Jiménez-Soto1, Sabine Clausen, Annika Sprenger

  • 1Max von Pettenkofer-Institute for Hygiene and Medical Microbiology, Ludwig-Maximilians-University, Pettenkoferstraße 9a, D-80336, Munich, Germany.

Cellular Microbiology
|July 13, 2013
PubMed

Insights

Previous Helicobacter pylori infection dose-dependently reduces CagA translocation by later strains. This interference by H. pylori is specific and mediated by outer membrane proteins, not other virulence factors.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Pathogenic Gram-negative bacteria use type IV secretion systems (T4SS) to inject effector proteins into host cells.
  • Helicobacter pylori utilizes the cag-T4SS to inject CagA into gastric epithelial cells, leading to signaling deregulation and gastric cancer.
  • CagA injection disrupts host cell functions, contributing to diseases like gastritis, ulcers, and cancer.

Purpose of the Study:

  • To investigate the effect of prior H. pylori infection on the CagA translocation efficiency of subsequent infections.
  • To elucidate the mechanisms and bacterial factors involved in this interference phenomenon.
  • To understand how H. pylori modulates host cell interactions to control effector delivery.

Main Methods:

  • Infection experiments using live H. pylori strains with varying pre-infection conditions.
  • Assessment of CagA translocation efficiency using quantitative assays.
  • Analysis of the role of T4SS, VacA, flagella, and specific outer membrane proteins (HopI, HopQ, AlpAB).
  • Testing interference by other bacterial species (E. coli, C. jejuni, S. aureus, lactobacilli).
  • Evaluation of β1 integrin receptor involvement.

Main Results:

  • Pre-infection with live H. pylori significantly and dose-dependently reduced CagA translocation by a subsequent infecting strain.
  • This interference was specific to H. pylori and not observed with other tested bacterial pathogens or commensals.
  • The effect was independent of H. pylori's T4SS, VacA, flagella, and β1 integrin receptor availability.
  • Specific outer membrane proteins, including HopI, HopQ, and AlpAB, were essential for mediating this interference.
  • The mechanism appears to be a host cell response controlled by H. pylori to limit CagA delivery.

Conclusions:

  • H. pylori establishes a specific interference mechanism that restricts CagA translocation by subsequent infections.
  • This self-regulation by H. pylori may serve to control host cell damage and modulate the host-pathogen interaction.
  • Outer membrane proteins play a crucial role in this novel interference pathway, distinct from known virulence factors.

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