Study on pathogenecity of Helicobacter pylori in gastroduodenum using germ-free mice.

无菌小鼠胃十二指肠幽门螺杆菌致病力研究。

• 批准号: 09670297
• 负责人: KAMIYA Shigeru
• 金额: $ 1.98万
• 依托单位: KYORIN UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670297/
• 关键词: H.Pylori; germ-free mouse; HSP60; adhesion; gastritis; プロバイオティクス; ヘリコプター・ピロリ; 胃十二指腸潰瘍; 病原因子

Germ-free (GF) mouse was orally infected with Helicobacter pylon TK1402 strain (10^<8-9> cfu/ 0.5 ml, three times). Persistent infection of H.pylon in gastric mucosa of the mouse was demonstrated from 1-9 weeks after the infection, and infiltration of inflammatory cells and partial atrophy of gastric mucosa was detected. These results indicate that GF mouse is a useful model for persistent H.pylon infection.Heat shock protein 60 (HSP6O) of H.pylon was shown to be associated with adhesion of H.pylon to gastric epithelial cells. Pretreatment of H.pylon with anti-HSP6O monoclonal antibody resulted in a significant decrease of the number of h. pylon colonized in gastric mucosa of CF mouse.Administration of HSP6O into gastric mucosa of GF mouse induced no significant gastric damage. In contrast, oral administration of HSP6O followed by challenge of H.pylon induced severe inflammatory change in the gastric mucosa. Interestingly, the number of H.pylon colonized was significantly lower by adminstration of HSP6O than that of control. Administration of imidazole derivatives or probiotics (Lactobacillus salivanius, Clostnidium butynicum) cured the persistent infection with H.pylon in CF mouse. These results indicate that GF mouse is also a useful model for evaluation of bactericidal drug or bacteriotherapy for H.pylon infection.

无菌丝（GF）小鼠口服用螺旋杆菌TK1402菌株感染（10^<8-8-9> CFU/ 0.5 ml，三次）。从感染后的1-9周证明了小鼠胃粘膜中h.抑制的持续感染，并检测到炎性细胞的浸润和胃粘膜的部分萎缩。这些结果表明，GF小鼠是持续性H.抑制感染的有用模型。H.β的热休克蛋白60（HSP6O）与H.酰基对胃皮细胞的粘附有关。用抗HSP6O单克隆抗体对H.抑制进行预处理，导致H数量显着减少。在CF小鼠的胃粘膜中定植的塔。将HSP6O施用到GF小鼠的胃粘膜中，不会引起明显的胃损伤。相比之下，口服HSP6O，然后挑战H.佩隆引起的胃粘膜炎症变化。有趣的是，通过HSP6O的构造，HSP6O殖民地的H.抑制殖民地的数量明显低于对照。咪唑衍生物或益生菌的给药（唾液乳杆菌，豆类丁氏菌）在CF小鼠中治愈了持续感染的H.佩隆。这些结果表明，GF小鼠也是评估杀菌剂药物或细菌疗法的有用模型。

项目成果

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林健二,他4名: "マウス感染モデルを用いたTY-50158のHelicobacter pyloriに対する除菌効果の検討," 無菌生物. 28(1). 72-74 (1998)

Kenji Hayashi 等人 4：“使用小鼠感染模型检查 TY-50158 对幽门螺杆菌的灭菌效果”，Germic Biol. 72-74 (1998)。

神谷 茂: "リコバクター. ピロリ感染症" 医薬ジャーナル社毒素産生菌とその感染症(竹田美文, 本田武司編), 255 (1998)

Shigeru Kamiya：“Lycobacter pylori感染”Iyaku Journal，产毒素细菌及其传染病（由Yoshifumi Takeda和Takeshi Honda编辑），255（1998）

Yamaguchi T et al: "Heat-shock protein 60 homologue of Helicobacter pylori is associated with adhesion of H.pyliri to human gastric epithelial cells" J Med Microbiol. 46 (10). 825-831 (1997)

Yamaguchi T 等人：“幽门螺杆菌的热休克蛋白 60 同源物与幽门螺杆菌对人胃上皮细胞的粘附有关”J Med Microbiol。