1997 Fiscal Year Final Research Report Summary
Establishment of Helicobacter pylori infection models in rats and mice
| Project/Area Number |
08557132
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Biological pharmacy
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| Research Institution | Kyoto Pharmaceutical University |
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Principal Investigator |
OKABE Susumu Kyoto Pharmaceutical University Department of Applied Pharmacology, Professor, 薬学部, 教授 (90012624)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Satoru Kyoto Pharmaceutical University Department of Applied Pharmacology, Research Ass, 薬学部, 助手 (20268098)
NISHINO Takeshi Kyoto Pharmaceutical University Department of Microbiology, Professor, 薬学部, 教授 (50097838)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Helicobacter pylori / infection / rat / mouse |
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| Research Abstract |
This study was designed to establish Helicobacter pylori (H.pylori) infection models in rats and mice. H.pylori of VacA-and CagA-positive strain (ATCC43504) was once orally inoculated to the animals. H.pylori infection was not observed in normal Donryu, Sprague-Dawley or Wistar rats. In contrast, the rats (Donryu strain) with gastric ulcers were infected with H.pylori. Gastric ulcers spontaneously healed, but H.pylori infection tended to impaire ulcer healing. The number of H.pylori in the stomach decreased with ulcer healing. Similarly, the rats (Sprague-Dawley strain) with HCl-induced mucosal lesions were infected with H.pylori. The number of H.pylori was associated with lesion area and decreased with the healing of the lesions. H.pylori infection did not affect the healing. On the other hand, in normal ddY mice, H.pylori persistently colonized the gastric mucosa for at least 26 weeks. The number of H.pylori was decreased by antibiotics such as amoxicillin and clarithromycin, and the antibiotics with proton pump inhibitors (omeprazole and lansoprazole) more profoundly reduced H.pylori viability in the stomach. H.pylori infection caused gastritis with inflammatory cell infiltration, but gastric pathology was mild, compared with those in H.pylori-infected humans and Mongolian gerbils. Even after H.pylori-infected mice were treated with aspirin, the pathology was not largely promoted. Gastric ulcers did not occur in H.pylori-infected mice.
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