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Development of animal model for enterohemorrhagic Escherichia coli infection

肠出血性大肠杆菌感染动物模型的建立

基本信息

批准号：
12670254
负责人：
YOH Myonsun
金额：
$ 2.11万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12670254/
关键词：
enterohemorrhagic E. coli animal model for infection O157 定着感染実験動物モデル

项目摘要

Infections due to Shiga toxin-producing Escherichia coli (STEC) are responsible for severe diarrheal diseases in humans, and these bacteria have recently emerged as a leading cause of renal failure and encephalitis in children and the aged. To develop rapid diagnosis methods or methods/medicines to treat patients infected with STEC, animal model are necessary. Conventional mice or rat are not sensitive for STEC. Gnotobiotic mice, antibiotics treated mice or malnutritional mice are used. Removal of the cecum from normal mice caused a major perturbation of the microbial ecology of the gastrointestinal tract. There was a permanent reduction in colonization resistance resulting in a 1,000-fold increase in the concentration of facultatively anaerobic coliform bacteria. Coincident with this increase in coliform counts was a decrease in the numbers of strictly anaerobic fusiform bacteria that dominate the rodent intestinal tract, resulting in reduced levels of volatile fatty acids. As the volatile fatty acids are major metabolic end products of anaerobic bacteria that colonize the rodent intestine and are produced mainly in the cecum, it was likely that the decrease in fatty acid levels was due to changes in the normal microbiota of the intestine. Cecectomized are likely to be a useful model for study of Intestinal pathogen that can not colonize in the intestine of normal mice. We succeeded to development of this model, though STEC challenged into cecectomized mice could not colonize and cause diarrea in challenged mice.

由产志贺毒素大肠杆菌（STEC）引起的感染是人类严重腹泻疾病的原因，这些细菌最近已成为儿童和老年人肾衰竭和脑炎的主要原因。为了开发快速诊断方法或治疗产志贺毒素大肠杆菌感染的方法/药物，有必要建立动物模型。常规小鼠或大鼠对产志贺毒素大肠杆菌不敏感。使用无糖生物小鼠、抗生素治疗小鼠或营养不良小鼠。从正常小鼠身上切除盲肠引起了胃肠道微生物生态的重大扰动。定植抗性永久性降低，导致兼性厌氧大肠菌群浓度增加1000倍。与大肠菌群数量增加相一致的是，在啮齿动物肠道中占主导地位的严格厌氧梭状细菌数量减少，导致挥发性脂肪酸水平降低。由于挥发性脂肪酸是啮齿动物肠道中定殖的厌氧菌的主要代谢终产物，主要在盲肠中产生，因此脂肪酸水平的下降可能是由于肠道正常菌群的变化所致。切除盲肠可能成为研究不能在正常小鼠肠道内定植的肠道病原体的有用模型。我们成功地开发了该模型，尽管大肠杆菌攻毒到切除盲肠的小鼠不能定植并引起攻毒小鼠腹泻。