期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 22, 期 2, 页码 619-629出版社
IOS PRESS
DOI: 10.3233/JAD-2010-100852
关键词
3xTg-AD Mice; Alzheimer's Disease; CCR6; inflammation
资金
- Department of Veterans' Affairs
- National Institutes of Health [NS45445, NS47661]
- Biomedical Laboratory R&D Service, Department of Veterans Affairs
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS047661, R01NS045445] Funding Source: NIH RePORTER
The inflammatory status of the brain in patients as well as animal models of Alzheimer's disease (AD) has been extensively studied. Accumulation of activated microglia producing tumor necrosis factor-alpha and monocyte chemotactic protein-1 contribute to the pathology of the disease. However, little is known about the changes in the spleen and associated peripheral immunity that might contribute to AD pathology. The goal of this study was to characterize phenotypic and functional changes in spleen, blood and brain cell populations that contribute to development of an AD-like disease in a triple transgenic (3xTg-AD) mouse model. The 3xTg-AD mice had increased percentages of brain Gr-1+ granulocytes, dendritic cells and macrophages, spleen and blood derived CD8+Ly6C+ memory T cells and CCR6+ B cells, as well as increased levels of secreted interleukin-6. Brain tissue from older 12 month old symptomatic 3xTg-AD female mice exhibited highly elevated mRNA expression of CCR6 compared to wild-type mice. Importantly, this pronounced increase in expression of CCR6 was also detected in brain and spleen tissue from pre-symptomatic 5-6 month old 3xTg-AD females and males. Our data demonstrate increased expression of CCR6 in the brain and peripheral immune organs of both pre-symptomatic and symptomatic 3xTg-AD mice, strongly suggesting an ongoing inflammatory process that precedes onset of clinical AD-like disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据