Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 2002 Mar;37(3):267-78.
doi: 10.1080/003655202317284165.

Differential susceptibility of inbred mouse strains to Helicobacter pylori infection

M Mähler  1 , C Janke, S Wagner, H J Hedrich
Affiliations
Comparative Study

Differential susceptibility of inbred mouse strains to Helicobacter pylori infection

M Mähler et al. Scand J Gastroenterol. 2002 Mar.

Abstract

Background: Host factors play an important part in the pathogenesis of Helicobacter pylori-associated disease. The aim of this study was to screen various inbred strains of mice for genetic differences in susceptibility to H. pylori infection.

Methods: Mice of strains BALB/cJ, C.B-17-Prkdc(scid), C3H/HeJ, C3H/HeN, C57BL/6J, C57BL/6J-I110(tm/Cgn), DBA/2J, and FVB/N were inoculated intragastrically with H. pylori SS1. At 1, 4 and 6 months after inoculation, mice were necropsied, and bacterial cultures and histologic studies of the stomachs were performed.

Results: Significant differences in the level of colonization by H. pylori were observed among inbred strains at each time of infection. These differences were most distinct at 4 months after inoculation with highest levels in strains C3H/HeJ and C3H/HeN and lowest in strains FVB/N, C57BL/6J and C57BL/6J-I110(tm/Cgn). Infected mice revealed a mild increase in inflammatory cells compared with controls at 1 and 4 months, but not at 6 months after inoculation. The host strain effect on gastric disease was fairly mild, with two exceptions. Firstly, infected I110(tm/Cgn) mice developed a severe, hyperplastic gastritis, indicating that interleukin-10 is an important regulator of the inflammatory response to H. pylori. Secondly, infected C3H/HeN mice had a propensity to develop lymphoid aggregates in the gastric mucosa.

Conclusions: The strain differences described here will be useful for the design of genetic mapping studies in mice to elucidate the genes controlling gastric infection by H. pylori. Our results further show that genetically altered mice are a valuable tool for identifying candidate genes possibly contributing to susceptibility to H. pylori infection.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

MeSH terms

LinkOut - more resources