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.