Proinflammatory profile of cytokine production by human monocytes and murine microglia stimulated with β-amyloid[25-35]

被引:133
作者
Meda, L
Baron, P
Prat, E
Scarpini, E
Scarlato, G
Cassatella, MA
Rossi, F
机构
[1] Univ Verona, Inst Gen Pathol, I-37134 Verona, Italy
[2] Univ Milan, Dino Ferrari Ctr, Inst Neurol, IRCCS,Osped Maggiore Policlin, I-20122 Milan, Italy
关键词
Alzheimer's disease; monocytes; microglia; beta-amyloid[25-35; cytokines; inflammation;
D O I
10.1016/S0165-5728(98)00188-X
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
Growing evidence indicates that amyloid (A beta) deposition and phagocyte activation participate in inflammatory reactions in the brain during the course of Alzheimer's disease. To further investigate the effects of A beta-phagocyte interaction, we examined the production of proinflammatory (IL-1 beta, IL-6), chemotactic (MIP-1 alpha, IP-10) and inhibitory (IL-1Ra, IL-10 and TGF beta(1)) cytokines by cultured human monocytes and mouse microglial cells upon stimulation with A beta[25-35]. Northern blot analysis and specific immunoassays demonstrated that A beta[25-35] triggers mRNA expression and release of IL-1 beta, IL-1Ra and MIP-1 alpha but not of IL-6, IL-10, TGF beta(1) and IP-10 from human monocytes. Similar results were obtained by examining the production of IL-1 beta, IL-6 and IL-10 from mouse microglial cells in the same experimental conditions. Taken together, these data indicate that AP-phagocyte interaction can drive a different response towards cytokine production by monocytes and microglia, with a particular proinflammatory trend, and further support a role for A beta deposition as a triggering factor of inflammatory events in Alzheimer's disease (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:45 / 52
页数:8
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