Role of Helicobacter pylori in the pathogenesis of gastric mucosa : long-term folow-up study in H.pylori infected Japanese macaques.

幽门螺杆菌在胃粘膜发病机制中的作用：幽门螺杆菌感染的日本猕猴的长期随访研究。

• 批准号: 05670487
• 负责人: FUJIOKA Toshio
• 金额: $ 1.09万
• 依托单位: Oita Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1993
• 资助国家: 日本
• 起止时间: 1993 至 1994
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05670487/
• 关键词: 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

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.

为了探讨幽门螺杆菌持续定植的致病作用，我们观察了幽门螺杆菌持续定植的病程延长和3年感染对胃粘膜的损害。采用本实验室建立的实验性胃炎模型，将幽门螺杆菌诱导的急性胃炎与未感染的对照组进行为期3年的比较。观察幽门螺杆菌的结肠率、胃炎积分、细胞内高碘酸席夫(PAS)阳性物质的体积和胃窦腺的高度，并与对照组比较。培养和组织学检查表明幽门螺杆菌持续定植。胃炎评分显著高于对照组，组织学结果与人类慢性活动性胃炎非常相似。同时，感染动物的PAS阳性物质含量和胃窦腺高度也显著下降。在本研究中，实验数据清楚地显示，感染的动物胃窦粘膜腺体高度明显降低，腺体体积也严重丧失。感染动物的胃窦细胞增殖显著增加。这些结果有力地表明，幽门螺杆菌的持续定植导致萎缩性胃炎，可能是导致胃癌的一系列事件的原因之一。

项目成果

Toshio Fujioka: "Experimental model for Chronic gastritis with Helicobacter pylori:-long-term follow-up study in H.pylori infected Japanese macagues.-" European Journal of Gastroenterology and Hepatology. 5. 73-77 (1993)

Toshio Fujioka：“幽门螺杆菌慢性胃炎的实验模型：幽门螺杆菌感染的日本猕猴的长期随访研究。”欧洲胃肠病学和肝脏病学杂志。

Toshio Fujioka: "Establishment of an animal model for chronic gostritis with Helicobacter pylori-Potential model for long-term observations-" European Journal of Gastrornterology and Hepatology. 6. 73-78 (1994)

Toshio Fujioka：“用幽门螺杆菌建立慢性胃炎动物模型 - 长期观察的潜力模型 -”欧洲胃肠病学和肝病学杂志。

R.SHUTO,T.FUJIOKA et al: "Experimental gastritis induced by Helicobacter pylori in Japanese monkeys." Intect.Immu.61. 933-939 (1993)

R.SHUTO,T.FUJIOKA 等人：“日本猴子中幽门螺杆菌诱发的实验性胃炎。”

T.FUJIOKA,T.KUBOTA et al: "Role of Helicobacter pylori in the progression of atroplic gastritis:experimental study." Development of Cancer Reseorch I. 41-52 (1994)

T.FUJIOKA、T.KUBOTA 等人：“幽门螺杆菌在萎缩性胃炎进展中的作用：实验研究”。

藤岡利生: "Helicobacter pylori 感染の動物モデル" Journal of Gastrointestinal Research. 2. 38-44 (1994)

Toshio Fujioka：“幽门螺杆菌感染的动物模型”胃肠研究杂志 2. 38-44 (1994)。