| Project/Area Number |
05670487
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Oita Medical University |
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Principal Investigator |
FUJIOKA Toshio Medicine, Oita Medical University, Assoc.Prof., 医学部, 助教授 (90145368)
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| Co-Investigator(Kenkyū-buntansha) |
KUBOTA Toshihiro Medicine, Oita Medical University, Instructor, 医学部, 助手 (30244172)
MURAKAMI Kazunari Medicine, Oita Medical University Instructor, 医学部, 助手 (00239485)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1994: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Helicobacter pylori / persistent colonization / atrophic gastritis / gastritis score / glandular height / Japanese monkey / 胃癌 / 萎縮性変化 / 壁細胞 / 増殖帯 |
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| Research Abstract |
To assess the pathogenic role of persisitent colonization with H.pylori, we investigated the extended serial course of H.pylori infection and the damage to the gastric mucosa caused by a 3-year infection.A cute gastritis induced by H.pylori using an experimental model established in our laboratory were compared with a non-infected control group for 3 years.Colonization by H.pylori, gastritis scores, volume of intracellular periodic acid-Schiff (PAS) -positive substances and the height of antral glands were investigated every 3 months for 3 years and compared with those of a control group.
In the infected group, persistent colonization with H.pylori was demonstrated by culture and histological examinations.Gastritis scores were significantly higher than those of the control group, and the histological findings were quite similar to those of chronic active gastritis observed in humans.Simultaneously, significant decreases in the contents of PAS-positive substances and in the height of antral glands were also demonstrated in infected animals.In the present study, experimental data clearly showed a significant decrease in glandular height in the antral mucosa of infected animals with severe loss of glandular volume also.Gastric antrum cell proliferation was significantly increased in the infected animals.These reaults strongly suggest that persistent colonization with H.pylori progress atrophic gastritis as a possible mechanism for a causal role in the chain of events leading to gastric carcinoma.
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