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Mouse Models Of Helicobacter Infection And Gastric Pathologies
07:43

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Published on: October 18, 2018

Helicobacter pylori induces an antimicrobial response in rhesus macaques in a cag pathogenicity island-dependent

Michael J Hornsby1, Jennifer L Huff, Robert J Kays

  • 1Department of Medical Microbiology & Immunology, University of California, Davis, Davis, California, USA.

Gastroenterology
|April 9, 2008
PubMed
Abstract

Insights

The cag pathogenicity island (cag PAI) of H pylori induces antimicrobial proteins, potentially aiding H pylori colonization and offering host protection. This study used a rhesus macaque model to investigate these effects.

Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Helicobacter pylori infection is a significant global health concern.
  • The cag pathogenicity island (cag PAI) is a key virulence factor in H. pylori.
  • Understanding host-pathogen interactions is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of the cag PAI in H. pylori host-pathogen interactions.
  • To determine the impact of the cag PAI on host gene expression and immune response.
  • To elucidate the function of the cag PAI in the gastric niche.

Main Methods:

  • Rhesus macaque model used for experimental H. pylori challenge.
  • Comparison of wild-type (WT) H. pylori strain J166 with its isogenic cag PAI knockout mutant.
  • Analysis of gastric biopsies via quantitative culture, histopathology, and host gene expression (microarray, RT-PCR, immunohistochemistry).

Main Results:

  • The cag PAI significantly influenced host gene expression, up-regulating innate antimicrobial effector proteins.
  • Key induced genes included elafin, siderocalin, DMBT1, DUOX2, and human-beta defensin-2 paralogues.
  • Inflammation and lamina propria expansion were attenuated in animals infected with the cag PAI knockout strain, indicating the cag PAI's role in modulating the host inflammatory response.

Conclusions:

  • The cag PAI induces a host antimicrobial response, potentially enhancing H. pylori's competitive advantage in the gastric environment.
  • This cag PAI-mediated response may offer a protective benefit to the host.
  • The findings provide insights into H. pylori pathogenesis and host adaptation strategies.

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