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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

Differential susceptibility of inbred mouse strains to Helicobacter pylori infection

M Mähler1, C Janke, S Wagner

  • 1Institute for Laboratory Animal Science and Central Animal Facility, Medical School Hannover, Germany. maehler.michael@mh-hannover.de

Scandinavian Journal of Gastroenterology
|March 28, 2002
PubMed
Abstract

Insights

Genetic differences in mouse strains significantly impact Helicobacter pylori infection levels and gastric disease. Specific strains like C3H/HeJ and FVB/N show varying susceptibility, aiding in the study of host factors in H. pylori pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Genetics

Background:

  • Host factors are crucial in Helicobacter pylori pathogenesis.
  • Understanding genetic susceptibility to H. pylori is vital for disease management.
  • This study investigates genetic variations in mouse models for H. pylori infection.

Purpose of the Study:

  • To screen inbred mouse strains for genetic differences in susceptibility to H. pylori infection.
  • To identify specific mouse strains exhibiting distinct responses to H. pylori SS1.
  • To lay the groundwork for genetic mapping studies to find genes controlling H. pylori gastric infection.

Main Methods:

  • Inoculation of eight inbred mouse strains (BALB/cJ, C.B-17-scid, C3H/HeJ, C3H/HeN, C57BL/6J, C57BL/6J-I110(tm/Cgn), DBA/2J, FVB/N) with H. pylori SS1.
  • Necropsy and analysis of gastric tissues at 1, 4, and 6 months post-inoculation.
  • Assessment of bacterial colonization levels and histological examination for inflammatory changes and disease markers.

Main Results:

  • Significant variations in H. pylori colonization levels were observed across mouse strains at all time points, most pronounced at 4 months.
  • Strains C3H/HeJ and C3H/HeN exhibited the highest colonization, while FVB/N, C57BL/6J, and C57BL/6J-I110(tm/Cgn) showed the lowest.
  • While most infected mice had mild inflammation, C57BL/6J-I110(tm/Cgn) mice developed severe gastritis, linked to interleukin-10 regulation, and C3H/HeN mice showed lymphoid aggregates.

Conclusions:

  • Observed strain differences in H. pylori susceptibility are valuable for designing genetic mapping studies.
  • Genetically modified mice serve as effective tools for identifying candidate genes influencing H. pylori infection susceptibility.
  • Interleukin-10 plays a key role in regulating the gastric inflammatory response to H. pylori.

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