Inoculation of VacA− and CagA− Helicobacter pylori Delays Gastric Ulcer Healing in the Rat

• Published in: Scandinavian journal of gastroenterology 1997, Vol.32 (5), p.439-444
• Main Authors: Li, H., Mellgård, B., Helander, H. F.
• Format: Article
• Language: English
• Subjects: Acetic Acid - toxicity; Animals; Antigens, Bacterial - genetics; Apoptosis; Bacterial Proteins - genetics; Biological and medical sciences; CagA; Cell Division; Disease Models, Animal; Duodenum - microbiology; Duodenum - pathology; Female; gastric epithelium; Gastric Mucosa - microbiology; Gastric Mucosa - pathology; Gastroenterology. Liver. Pancreas. Abdomen; Helicobacter Infections - microbiology; Helicobacter Infections - pathology; Helicobacter pylori; Helicobacter pylori - genetics; Helicobacter pylori - pathogenicity; Immunohistochemistry; labelling index; Medical sciences; Other diseases. Semiology; Phenotype; rat; Rats; Rats, Sprague-Dawley; Stomach Ulcer - chemically induced; Stomach Ulcer - microbiology; Stomach Ulcer - pathology; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; ulcer healing; VacA; Wound Healing
• ISSN: 0036-5521; 1502-7708
• DOI: 10.3109/00365529709025078

Background: Helicobacter pylori is associated with peptic ulcer disease. In the present study, the influence of VacA and CagA− H. pylori on gastric ulcer healing was studied in the rat. Methods: Twenty-four rats with acetic-acid-induced gastric ulcer were divided into two groups and given either vehicle (Brucella broth) or H. pylori suspension by gavage every 12 h for 7 days. The animals were killed 1 and 8 days after the last H. pylori gavage (i.e. 10 and 17 days after the induction of the ulcer). One hour before death, 3H-thymidine was given intraperitoneally. Tissue samples from the stomach (including the ulcer area) and the duodenum were processed for determination of labelling index and apoptotic cells. Results: Compared with the vehicle-treated controls, the ulcer area in H. pylori-inoculated rats was significantly larger, the epithelial apoptotic cells in the ulcer margin and intact corpus were more numerous, while the cell proliferation of gastroduodcnal epithelium was slightly, but not significantly, increased by H. pylori gavage. Conclusion: Gastric ulcer healing was delayed after the inoculation of VacA− and CagA H. pylori in the rat, possibly as a result of excess cell loss by apoptosis.