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Volume 53, Number 3-4 >

Alymphoplasia mice are resistant to prion infection via oral route

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この文献には次のDOIがあります:http://doi.org/10.14943/jjvr.53.3-4.149

タイトル: Alymphoplasia mice are resistant to prion infection via oral route
著者: Horiuchi, Motohiro 著作を一覧する
Furuoka, Hidefumi 著作を一覧する
Kitamura, Nobuo 著作を一覧する
Shinagawa, Morikazu 著作を一覧する
キーワード: prion
scrapie
alymphoplasia
GALT
発行日: 2006年 2月28日
出版者: The Graduate School of Veterinary Medicine, Hokkaido University
誌名: Japanese Journal of Veterinary Research
巻: 53
号: 3-4
開始ページ: 149
終了ページ: 157
抄録: The major cause of infection in animal prion diseases is thought to be consumption of prion-contaminated stuff. There is evidence that the enteric nerve system (ENS) and gut-associated lymphoid tissues (GATL) are involved in the establishment of prion infection through alimentary tract. To elucidate the initial entry port for prion, we inoculated prion to alymphoplasia (aly ) mice showing a deficiency in systemic lymph nodes and Peyer’s patches. The aly /aly mice were susceptible to prion infection by intra-cranial inoculation and there were no differences in incubation periods between aly/aly mice and wild-type C57BL/6J mice. Incubation periods in aly/aly mice were about20 days longer than those in C57BL/6J mice with the intra-peritoneal inoculation. The aly /aly mice were completely resistant to prion infection by per os administration, while C57BL/6J mice were sensitive as they entered the terminal stage of disease around300days post inoculation. PrPSc were detected in the intestine and spleen of C57BL/6J mice inoculated with prion intraperitoneally or orally ; however PrPSc was not detected in the spleen and intestine of aly /aly mice. Prion infectivity was detected in the intestines and spleens of prion-inoculated C57BL/6J mice, even after the early stages of exposure, while no infectivity was detected in these tissues of prion-inoculated aly /aly mice. No apparent differences were observed in the organization of the enteric nerve system between wild-type and aly /aly mice. These results indicate that GALT rather than ENS acts as the primary entry port for prion after oral exposure. 1)Laboratory of Prion Diseases, Graduate
資料タイプ: bulletin
URI: http://hdl.handle.net/2115/5935
出現コレクション:Volume 53, Number 3-4

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