Effects of immunomodulatory substances on phagocytosis of A β 1-42 by human microglia

Marianne Schultzberg, Erik Hjorth, Dan Frenkel, Howard Weiner

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Glial activation and increased inflammation characterize neuropathology in Alzheimer's disease (AD). The aim was to develop a model for studying phagocytosis of β-amyloid (Aβ) peptide by human microglia and to test effects thereupon by immunomodulatory substances. Human CHME3 microglia showed intracellular A β1-42 colocalized with lysosome-associated membrane protein-2, indicating phagocytosis. This was increased by interferon-, and to a lesser degree with Protollin, a proteosome-based adjuvant. Secretion of brain-derived neurotrophic factor (BDNF) was decreased by A β1-42 and by interferon- and interleukin-1. These cytokines, but not A β1-42, stimulated interleukin-6 release. Microglia which phagocytosed β1-42 exhibited a higher degree of expression of interleukin-1 receptor type I and inducible nitric oxide synthase. In conclusion, we show that human microglia are able to phagocytose A β1-42 and that this is associated with expression of inflammatory markers. A β1-42 and interferon- decreased BDNF secretion suggesting a new neuropathological role for A β1-42 and the inflammation accompanying AD.

Original languageEnglish
Article number798424
JournalInternational Journal of Alzheimer's Disease
StatePublished - 2010


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