A rat model of chronic Helicobacter pylori infection. Studies of epithelial cell turnover and gastric ulcer healing

Scand J Gastroenterol. 1998 Apr;33(4):370-8. doi: 10.1080/00365529850170991.

Abstract

Background: Our aim was to infect rats with Helicobacter pylori and to study the effects of the infection on the gastric mucosa in normal and in ulcer-operated rats.

Methods: A mouse-adapted H. pylori (cagA-, VacA-) strain was inoculated into 23 rats. Another 20 uninfected rats served as controls. Two months later a gastric ulcer was induced in some rats. The animals were killed 3, 6, or 15 days after the ulcer operation. Tissues were taken for histology and for culture of H. pylori. Serum antibodies were determined.

Results: All inoculated rats were infected by H. pylori after 2 months, mainly in the antrum. In these rats a mild to moderate chronic inflammation and a significantly increased frequency of apoptotic cells were observed in the antrum and in the ulcer margin, the ulcer healing was delayed, and the serum level of H. pylori-specific Ig was increased.

Conclusions: H. pylori infection in rats was successful and was accompanied by a mild to moderate mucosal inflammation. Gastric ulcer healing was delayed in infected rats, probably due to the inflammation and the increased apoptosis in epithelium.

MeSH terms

  • Animals
  • Apoptosis
  • Cell Division
  • Disease Models, Animal
  • Enzyme-Linked Immunosorbent Assay
  • Epithelial Cells / cytology
  • Gastric Mucosa / microbiology*
  • Gastric Mucosa / pathology
  • Gastric Mucosa / physiopathology
  • Gastritis / microbiology*
  • Gastritis / pathology
  • Gastritis / physiopathology
  • Helicobacter Infections / pathology*
  • Helicobacter Infections / physiopathology
  • Helicobacter pylori* / growth & development
  • Male
  • Mice
  • Rats
  • Rats, Sprague-Dawley
  • Stomach Ulcer / chemically induced
  • Stomach Ulcer / pathology
  • Stomach Ulcer / physiopathology*
  • Wound Healing / physiology*