N-truncation and pyroglutaminylation enhances the opsonizing capacity of AÎ²-peptides and facilitates phagocytosis by macrophages and microglia

Article ID	Journal	Published Year	Pages	File Type
7281516	Brain, Behavior, and Immunity	2014	10 Pages	PDF

Abstract

Taken together, AÎ²-peptides support phagocytosis as soluble factors and act as opsonins. Differential effects among the AÎ²-peptide variants point to distinct mechanisms of interaction among monocytes/macrophages, prey and AÎ²-peptides. A proinflammatory polarization induced by the phagocytosis of AÎ²-peptide coated particles may provide a model for the chronic inflammatory reaction and sustained plaque deposition in AD.

Keywords

PSP rhM-CSF rhGM-CSF sAPPα Phorbol-12-myristate-13-acetate MACS sAPPβ PRR TLR FCS APP DAPI iNOS DAMP Aβ E. coli PBS PBMC MFI 4′,6-diamidino-2-phenylindole BSA PMA bovine serum albumin amyloid-β EDTA Ethylenediaminetetraacetic acid Escherichia coli Neuroinflammation damage-associated molecular pattern Opsonization Alzheimer’s disease Toll-like receptor CNS Polystyrene particle fetal calf serum Peripheral blood mononuclear cell inducible nitric oxide synthase central nervous system Phagocytosis Macrophage polarization Macrophage Phosphate-buffered saline Monocyte mean fluorescent intensity amyloid precursor protein pattern recognition receptor