Smits Hessel A, Rijsmus Annemarie, van Loon Joyce H, Wat Jesse W Y, Verhoef Jan, Boven Leonie A, Nottet Hans S L M
Section Neuroimmunology, Eijkman-Winkler Institute for Microbiology, Infectious Diseases and Inflammation, University Medical Center Utrecht, Heidelberglaan 100, NL-3584 CX Utrecht, The Netherlands.
J Neuroimmunol. 2002 Jun;127(1-2):160-8. doi: 10.1016/s0165-5728(02)00112-1.
In Alzheimer's disease (AD), chemotaxis might be responsible for attracting glial cells towards the neuritic plaque. Using primary monocyte-derived macrophages and primary adult astrocytes as a model, amyloid-beta (Abeta) (1-42) was able to stimulate the production, as measured by RT-PCR, of MIP-1alpha and MIP-1beta mRNA in macrophages and MCP-1 in astrocytes. Cocultures showed in unstimulated as well as in Abeta-stimulated cells an increase in MIP-1alpha, MIP-1beta and MCP-1 mRNA. ELISAs of supernatant samples of stimulated macrophages and astrocytes also showed an increase in MIP-1alpha and MIP-1beta in macrophages and MCP-1 in astrocytes. Stimulated cocultures showed an increase in MIP-1alpha, MIP-1beta and MCP-1 protein levels in contrast to unstimulated cocultures.
在阿尔茨海默病(AD)中,趋化作用可能是导致神经胶质细胞向神经炎性斑块趋化的原因。以原代单核细胞衍生的巨噬细胞和原代成年星形胶质细胞为模型,通过逆转录聚合酶链反应(RT-PCR)检测发现,β淀粉样蛋白(Aβ)(1-42)能够刺激巨噬细胞产生巨噬细胞炎性蛋白-1α(MIP-1α)和巨噬细胞炎性蛋白-1β(MIP-1β)的信使核糖核酸(mRNA),并刺激星形胶质细胞产生单核细胞趋化蛋白-1(MCP-1)。共培养实验表明,在未受刺激以及Aβ刺激的细胞中,MIP-1α、MIP-1β和MCP-1的mRNA均有所增加。对受刺激的巨噬细胞和星形胶质细胞的上清液样本进行酶联免疫吸附测定(ELISA),结果也显示巨噬细胞中的MIP-1α和MIP-1β以及星形胶质细胞中的MCP-1有所增加。与未受刺激的共培养物相比,受刺激的共培养物中MIP-1α、MIP-1β和MCP-1的蛋白水平有所增加。