Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (8): 872-877.doi: 10.4103/1673-5374.131605

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

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

  1. Department of Neurology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
  • Received:2014-02-25 Online:2014-04-25 Published:2014-04-25
  • Contact: Yunpeng Cao, Ph.D., Department of Neurology, First Affiliated Hospital of China Medical University, Shenyang 110005, Liaoning Province, China
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 30471927.

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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.