β-amyloid fragment potentiates IL-6 and TNF-α secretion by LPS in astrocytes but not in microglia

Gianluigi Forloni, Fabio Mangiarotti, Nadia Angeretti, Elisa Lucca, Maria Grazia De Simoni

Research output: Contribution to journalArticlepeer-review

Abstract

The effect of a peptide homologous to the biologically active fragment of β amyloid 25-35 (β 25-35) was studied on interleukin 6 (IL-6) and tumour necrosis factor (TNF-α) secretion induced by lipopolysacharide (LPS) in primary rat astrocytes and microglia. Twenty-four hour exposure to LPS (50 ng/ml) induced IL-6 and TNF-α both in astrocytes and in microglial cells, while the effect of β 25-35 (50 μM) per se was negligible in both cell types. In microglial cells, the application of β peptide did not alter the production of either cytokine induced by LPS. However, β 25-35 strongly amplified the production of both IL-6 and TNF-α in astrocytes. These findings confirm the complex interaction between cytokines and amyloidogenesis in Alzheimer's disease and indicate that astrocytes rather than microglia respond to the β amyloid fragment, suggesting that these cells may be actively involved in cytokine-mediated events in AD.

Original languageEnglish
Pages (from-to)759-762
Number of pages4
JournalCytokine
Volume9
Issue number10
DOIs
Publication statusPublished - Oct 1997

Keywords

  • β-amyloid
  • Alzheimer's disease
  • Astrocytes
  • IL-6
  • TNF

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Immunology
  • Immunology and Allergy

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