In the present study we have examined the ability of the beta-amyloid peptide (A beta(25-35)) to modulate the respiratory burst activity of human monocytes in vitro. Incubation of the cells for 24 h with A beta(25-35) as well as with A beta(1-42) resulted in an enhanced production of reactive oxygen radicals (ROI) in response to phorbol 12-myristate 13-acetate (PMA). Such effect was additively increased by coincubation with interferon-gamma (IFN gamma), and was paralleled by modulation of gene and protein expression of some components of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system. Since the effects of A beta(25-35) were also reproduced in primary rat microglia, our findings indicate that A beta(25-35) can potentiate the ability of mononuclear phagocytes to produce ROI, and add further insights into its biological effects.
Priming of monocyte respiratory burst by beta-amyloid fragment (25-35)
ROSSI, Filippo;CASSATELLA, Marco Antonio
1996-01-01
Abstract
In the present study we have examined the ability of the beta-amyloid peptide (A beta(25-35)) to modulate the respiratory burst activity of human monocytes in vitro. Incubation of the cells for 24 h with A beta(25-35) as well as with A beta(1-42) resulted in an enhanced production of reactive oxygen radicals (ROI) in response to phorbol 12-myristate 13-acetate (PMA). Such effect was additively increased by coincubation with interferon-gamma (IFN gamma), and was paralleled by modulation of gene and protein expression of some components of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system. Since the effects of A beta(25-35) were also reproduced in primary rat microglia, our findings indicate that A beta(25-35) can potentiate the ability of mononuclear phagocytes to produce ROI, and add further insights into its biological effects.
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