Priming of monocyte respiratory burst by β-amyloid fragment (25–35)

• Published in: Neuroscience letters Vol. 219; no. 2; pp. 91 - 94
• Main Authors: Meda, Lucia, Bonaiuto, Corrada, Baron, Pierluigi, Otvos, Laszlo, Rossi, Filippo, Cassatella, Marco Antonio
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 22.11.1996; Elsevier
• Subjects: Amyloid beta-Peptides - pharmacology; Animals; Biological and medical sciences; Blotting, Northern; Blotting, Western; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Homeostasis; Humans; Immunobiology; Interferon-gamma - pharmacology; Microglia; Microglia - drug effects; Microglia - physiology; Monocytes; Monocytes - drug effects; Monocytes - physiology; Monocytes, macrophages; Myeloid cells: ontogeny, maturation, markers, receptors; NADPH Oxidases - metabolism; Nicotinamide adenine dinucleotide phosphate oxidase; Peptide Fragments - pharmacology; Rats; Reactive Oxygen Species - metabolism; Respiratory burst; Respiratory Burst - drug effects; RNA, Messenger - metabolism; β-Amyloid (25–35); Nicotinamide adenine dinucleotide phosphate oxidase; Monocytes; β-Amyloid (25–35); Respiratory burst; Microglia; Human; Monocyte; Peptide fragment; Immunomodulation; β Amyloid protein; Neuroglia; Priming; In vitro; Phagocyte
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(96)13177-3

In the present study we have examined the ability of the β-amyloid peptide (Aβ(25–35)) to modulate the respiratory burst activity of human monocytes in vitro. Incubation of the cells for 24 h with Aβ(25–35) as well as with Aβ(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-γ (IFNγ), 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 Aβ(25–35) were also reproduced in primary rat microglia, our findings indicate that Aβ(25–35) can potentiate the ability of mononuclear phagocytes to produce ROI, and add further insights into its biological effects.