Differential Susceptibility of Inbred Mouse Strains to Helicobacter pylori Infection

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- Il10 tm1Cgn , 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- Il10 tm1Cgn. 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 Il10 tm1Cgn 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.

• Colonization
• Genetic Predisposition
• Helicobacter
• Pylori
• Host Factors
• Inflammation
• Interleukin
• Mouse Model