Nasal mucosal inhalation of amyloid-beta peptide 3-10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid （1-42）

Three-month-old Alzheimer＇s disease model transgenic mice were immunized with Aβ1-42, Plp-Adenovirus [Ad]-X-CMV-（Aβ3-10）lo-CpG [AdCpG-（Aβ3-10）1] or AdCpG virus fluid via na- sal mucosal inhalation, respectively. ELISA analysis of serum showed Aβ42 antibody titers were significantly increased in mice...

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Bibliographic Details
Published in:中国神经再生研究：英文版 2014, Vol.9 (8), p.872-877
Main Author: Tongzi Jiang Wanshu Guo Sha Sha Xiaona Xing Rong Guo Yunpeng Cao
Format: Article
Language:English
Subjects:
IL-10
β-淀粉样蛋白
伴刀豆球蛋白A
缺陷型
腺病毒
转基因小鼠
酶联免疫吸附分析
阿尔茨海默氏症
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Summary:Three-month-old Alzheimer＇s disease model transgenic mice were immunized with Aβ1-42, Plp-Adenovirus [Ad]-X-CMV-（Aβ3-10）lo-CpG [AdCpG-（Aβ3-10）1] or AdCpG virus fluid via na- sal mucosal inhalation, respectively. ELISA analysis of serum showed Aβ42 antibody titers were significantly increased in mice immunized with Aβ1-42 and AdCpG-（Aβ3-10）10. Concanavalin A and AdCpG-（Aβ3-10）10 stimulation significantly increased the number of proliferating spleen cells cultured from AdCpG（Aβ3-10）Io and Aβ42 groups compared with the control group. In the AdCp- G（Aβ3-10）10 group, levels of interleukin （IL）-4 and IL-10 were increased, while those of IL-2 and interferon-y were decreased. In the A[342 group, levels of IL-4, IL-10, IL-2 and interferon-y were all increased. Experimental findings indicate that AdCpG-（Aβ3-10）10 vaccine can produce strong T helper 2 （Th2） humoral immune responses in addition to the production of Aβ42 antibody. The cellular immunologic response was weak and avoided Aβ1-42-mediated cytotoxicity.
ISSN:1673-5374