Amyloid-β-induced chemokine production in primary human macrophages and astrocytes

被引：126

作者：

Smits, HA ^{[1
]}

Rijsmus, A ^{[1
]}

van Loon, JH ^{[1
]}

Wat, JWY ^{[1
]}

Verhoef, J ^{[1
]}

Boven, LA ^{[1
]}

Nottet, HSLM ^{[1
]}

机构：

[1] Univ Utrecht, Med Ctr, Sect Neuroimmunol, Eijkman Winkler Inst Microbiol Infect Dis & Infla, NL-3584 CX Utrecht, Netherlands

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2002年 / 127卷 / 1-2期

关键词：

Alzheimer's disease; chemotaxis; glial cells; cell-to-cell interactions; chemokines;

D O I：

10.1016/S0165-5728(02)00112-1

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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 A beta-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. (C) 2002 Elsevier Science B.V. All rights reserved.

引用

页码：160 / 168

页数：9

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