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

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	Nasal mucosal inhalation of amyloid-beta peptide 3-10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1-42)
其他题名	Nasal mucosal inhalation of amyloid-beta peptide 3–10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1–42)
	Jiang Tongzi; Guo Wanshu; Sha Sha; Xing Xiaona; Guo Rong; Cao Yunpeng
	2014
发表期刊	NEURAL REGENERATION RESEARCH
ISSN	1673-5374
卷号	9 期号:8 页码:872-877
摘要	Three-month-old Alzheimer's disease model transgenic mice were immunized with A beta Plp-Adenovirus Ad-X-CMV-(A beta(3-10))(10)-CpG AdCpG-(A beta(3-10))(10) or AdCpG virus fluid via nasal mucosal inhalation, respectively. ELISA analysis of serum showed A beta(42) antibody titers were significantly increased in mice immunized with A beta(1-42) and AdCpG-(A beta(3-10))(10). Concanavalin A and AdCpG-(A beta(3-10))(10) stimulation significantly increased the number of proliferating spleen cells cultured from AdCpG(A beta(3-10))(10) and A beta(42) groups compared with the control group. In the AdCpG(A beta(3-10))(10) group, levels of interleukin (IL)-4 and IL-10 were increased, while those of IL-2 and interferon-gamma were decreased. In the A beta(42) group, levels of IL-4, IL-10, IL-2 and interferon-gamma were all increased. Experimental findings indicate that AdCpG-(A beta(3-10))(10) vaccine can produce strong T helper 2 (Th2) humoral immune responses in addition to the production of A beta(42) antibody. The cellular immunologic response was weak and avoided A beta(1-42)-mediated cytotoxicity.
其他摘要	Three-month-old Alzheimer's disease model transgenic mice were immunized with Aβ 1–42 Plp-Adenovirus Ad-X-CMV-(Aβ 3–10 ) 10 -CpG AdCpG-(Aβ 3–10 ) 10 or AdCpG virus fluid via nasal mucosal inhalation, respectively. ELISA analysis of serum showed Aβ 42 antibody titers were significantly increased in mice immunized with Aβ 1–42 and AdCpG-(Aβ 3–10 ) 10 . Concanavalin A and AdCpG-(Aβ 3–10 ) 10 stimulation significantly increased the number of proliferating spleen cells cultured from AdCpG(Aβ 3–10 ) 10 and Aβ 42 groups compared with the control group. In the AdCpG(Aβ 3–10 ) 10 group, levels of interleukin (IL)-4 and IL-10 were increased, while those of IL-2 and interferon-γ were decreased. In the Aβ 42 group, levels of IL-4, IL-10, IL-2 and interferon-γ were all increased. Experimental findings indicate that AdCpG-(Aβ 3–10 ) 10 vaccine can produce strong T helper 2 (Th2) humoral immune responses in addition to the production of Aβ 42 antibody. The cellular immunologic response was weak and avoided Aβ 1–42 -mediated cytotoxicity.
关键词	ALZHEIMERS-DISEASE TRANSGENIC MICE TANDEM REPEATS MOUSE MODEL IMMUNIZATION VACCINATION MEMORY IMMUNOTHERAPY ANTIBODIES DECLINE nerve regeneration neurodegenerative disease Alzheimer's disease immunotherapy amyloid-beta peptide vaccine cytokines humoral immunity inflammation NSFC grant neural regeneration
收录类别	CSCD
语种	英语
资助项目	[National Natural Science Foundation of China]
CSCD记录号	CSCD:5135520
引用统计
文献类型	期刊论文
条目标识符	http://ir.imr.ac.cn/handle/321006/143059
专题	中国科学院金属研究所
作者单位	中国科学院金属研究所
推荐引用方式 GB/T 7714	Jiang Tongzi,Guo Wanshu,Sha Sha,et al. Nasal mucosal inhalation of amyloid-beta peptide 3-10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1-42)[J]. NEURAL REGENERATION RESEARCH,2014,9(8):872-877.
APA	Jiang Tongzi,Guo Wanshu,Sha Sha,Xing Xiaona,Guo Rong,&Cao Yunpeng.(2014).Nasal mucosal inhalation of amyloid-beta peptide 3-10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1-42).NEURAL REGENERATION RESEARCH,9(8),872-877.
MLA	Jiang Tongzi,et al."Nasal mucosal inhalation of amyloid-beta peptide 3-10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1-42)".NEURAL REGENERATION RESEARCH 9.8(2014):872-877.