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

鼻粘膜吸入淀粉样β肽3-10缺陷腺病毒可减弱β淀粉样蛋白(1-42)诱导的细胞毒性

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作者:Tongzi Jiang, Wanshu Guo, Sha Sha, Xiaona Xing, Rong Guo, Yunpeng Cao

Abstract

Three-month-old Alzheimer's disease model transgenic mice were immunized with Aβ1-42 Plp-Adenovirus [Ad]-X-CMV-(Aβ3-10)10-CpG [AdCpG-(Aβ3-10)10] or AdCpG virus fluid via nasal 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)10 and Aβ42 groups compared with the control group. In the AdCpG(Aβ3-10)10 group, levels of interleukin (IL)-4 and IL-10 were increased, while those of IL-2 and interferon-γ were decreased. In the Aβ42 group, levels of IL-4, IL-10, IL-2 and interferon-γ 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.

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