Journal
JOURNAL OF NEUROCHEMISTRY
Volume 94, Issue 2, Pages 289-298Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1471-4159.2005.03188.x
Keywords
amyloid beta 1-40 peptide; cytosin-guanosin oligodesoxynucleotide; lipopolysaccharide; microglia; nitric oxide; tripalmytoyl-cysteinyl-seryl-(lysyl)3-lysine
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The interaction of endogenous and exogenous stimulators of innate immunity was examined in primary cultures of mouse microglial cells and macrophages after application of defined Toll-like receptor (TLR) agonists [lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide Pam3Cys-Ser-Lys4 (Pam3Cys) (TLR2) and single-stranded unmethylated CpG-DNA (CpG) (TLR9)] alone and in combination with amyloid beta peptide (Abeta) 1-40. Abeta 1-40 stimulated microglial cells and macrophages primed by interferon-gamma in a dose-dependent manner. Co-administration of Abeta1-40 with LPS or Pam3Cys led to an additive release of nitric oxide (NO) and tumour necrosis factor alpha (TNF-alpha). This may be one reason for the clinical deterioration frequently observed in patients with Alzheimer's disease during infections. In contrast, co-application of Abeta1-40 with CpG led to a substantial decrease of NO and TNF- alpha release compared with stimulation with CpG alone. Abeta 1-40 and CpG did not co-localize within the same subcellular compartment, making a direct physicochemical interaction as the cause of the observed antagonism very unlikely. This suggests that not all TLR agonists enhance the stimulatory effect of Abeta on innate immunity.
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