The Helicobacter felis Mouse Model in Assessing Anti-Helicobacter Therapies and Gastric Mucosal Prostaglandin E₂ Levels

Abstract

Background: The aims of the present study were to assess the usefulness of the Helicobacter felis mouse model in the evaluation of antimicrobial therapies and the effect of Helicobacter infection on gastric mucosal prostaglandin E₂ release. Methods: Barrier-maintained BALB/c mice were infected with H. felis and treated with different antibacterial therapies. H. felis status was determined by bacterial culture, urease test, and bacterial and histologic stainings. Release of prostaglandin E₂ from the gastric mucosa was measured by radioimmunoassay. Results: All triple-treated mice were cleared of bacteria both 24 h and 1 month after treatment. However, tinidazole alone also resulted in 100% eradication. Monotherapies with erythromycin acistrate, tetracycline, colloidal bismuth subcitrate, and nitecapone failed to eradicate the bacteria. The release of gastric prostaglandin E₂ was doubled in the infected mice (554 ± 39, mean ± SE) compared with the noninfected mice (270 ± 35) (p < 0.01). Conclusions: The H. felis mouse model proved satisfactory for assessing both anti-Helicobacter therapies and the prostaglandin E₂ release. The reliability of this method was improved when several methods to assess the H. felis status were used in parallel.

Key Words:

• Anti-Helicobacter therapy
• Helicobacter felis
• Helicobacter pylori
• mouse model
• prostaglandin E₂