implication of the structure of the Helicobacter pylori cag pathogenicity island in induction of interleukin-8

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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

C Audibert1, C Burucoa, B Janvier

  • 1Laboratoire de Microbiologie A, CHU La Milétrie, 86021 Poitiers Cedex, France.

Infection and Immunity
|February 17, 2001
PubMed

Insights

The cag pathogenicity island (PAI) structure is conserved in Helicobacter pylori and linked to interleukin-8 (IL-8) secretion, a key factor in gastric inflammation. However, some strains induce IL-8 independently of the cag PAI.

Area of Science:

  • Microbiology
  • Genetics
  • Immunology

Background:

  • Helicobacter pylori virulence is linked to the cag pathogenicity island (PAI).
  • The cag PAI influences interleukin-8 (IL-8) secretion, crucial for gastric inflammation during H. pylori infection.

Purpose of the Study:

  • To investigate the genetic conservation of the cag PAI.
  • To determine the association between cag PAI structure and IL-8 induction ability.

Main Methods:

  • PCR and dot blot hybridization for specific marker detection (cagA, picB, cag13-cag14, virD4, IS605).
  • Long-distance PCR to assess cagI, cagII, and middle regions of the cag PAI.
  • Coculture of H. pylori strains with HEp-2 cells to evaluate IL-8 induction.

Main Results:

  • 54.3% of 153 strains had an intact cag PAI; 32% lacked it.
  • An intact cag PAI correlated with IS605 presence and IL-8 secretion ability (P = 0.006).
  • Clinical presentation (ulcers vs. gastritis) was not linked to cag PAI structure.

Conclusions:

  • The cag PAI structure is relatively conserved and influences H. pylori's proinflammatory potential.
  • While the cag PAI is a major driver of IL-8 secretion, other factors may also contribute.

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