Bacterial infection promotes colon tumorigenesis in Apc(Min/+) mice

J Infect Dis. 2001 Jul 15;184(2):227-30. doi: 10.1086/321998. Epub 2001 Jun 18.

Abstract

The Min mouse, which has a germ line mutation in 1 allele of the Apc tumor suppressor gene, is a model for the early steps in human colorectal cancer. Helicobacter pylori infection, a known risk factor for gastric cancer in humans, causes chronic inflammation and increased epithelial cell proliferation in the stomach. Infection with the bacterium Citrobacter rodentium is known to increase epithelial cell proliferation and to promote chemically initiated tumors in the colon of mice. Min mice infected with C. rodentium at 1 month of age were found to have a 4-fold increase in the number of colonic adenomas at 6 months of age, compared with uninfected Min mice. Most of the colonic adenomas in the infected Min mice were in the distal colon, where C. rodentium-induced hyperplasia occurs. These data demonstrate that bacterial infection promotes colon tumor formation in genetically susceptible mice.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenoma / enzymology
  • Adenoma / microbiology*
  • Adenoma / pathology
  • Alleles
  • Animals
  • Cell Division
  • Citrobacter freundii*
  • Colon / enzymology
  • Colon / microbiology*
  • Colon / pathology*
  • Colonic Neoplasms / enzymology
  • Colonic Neoplasms / microbiology*
  • Colonic Neoplasms / pathology
  • Cyclooxygenase 2
  • Disease Models, Animal
  • Enterobacteriaceae Infections / complications*
  • Enterobacteriaceae Infections / enzymology
  • Enterobacteriaceae Infections / microbiology
  • Enterobacteriaceae Infections / pathology
  • Epithelial Cells / enzymology
  • Epithelial Cells / microbiology
  • Epithelial Cells / pathology
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Neoplastic
  • Genes, APC / genetics*
  • Germ-Line Mutation
  • Hyperplasia
  • Immunohistochemistry
  • Isoenzymes / analysis*
  • Mice
  • Mice, Inbred Strains
  • Peroxidases / analysis
  • Prostaglandin-Endoperoxide Synthases / analysis*
  • Risk Factors

Substances

  • Isoenzymes
  • Peroxidases
  • Cyclooxygenase 2
  • Prostaglandin-Endoperoxide Synthases