CXCL8 protects human neurons from amyloid-β-induced neurotoxicity: Relevance to Alzheimer's disease

Ashutosh, Wei Kou, Robin Cotter, Kathleen Borgmann, Li Wu, Raisa Persidsky, Namita Sakhuja, Anuja Ghorpade

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Alzheimer's disease (AD) is a neurodegenerative disease characterized by amyloid-β (Aβ) deposition in senile plaques colocalized with activated microglia and astrocytes. Recent studies suggest that CXCL8 is involved in the AD pathogenesis. The objective of this study was to determine the cellular sources of CXCL8 in the central nervous system during AD pathogenesis, and investigate the effects of CXCL8 on neuronal survival and/or functions. Our results showed significantly higher CXCL8 levels in AD brain tissue lysates as compared to those of age-matched controls. Upon Aβ and/or pro-inflammatory cytokine stimulation, microglia, astrocytes and neurons were all capable of CXCL8 production in vitro. Although CXCL8-alone did not alter neuronal survival, it did inhibit Aβ-induced neuronal apoptosis and increased neuronal brain-derived neurotrophic factor (BDNF) production. We conclude that microglia, astrocytes and neurons, all contribute to the enhanced CXCL8 levels in the CNS upon Aβ and/or pro-inflammatory cytokine stimulation. Further, CXCL8 protects neurons possibly by paracrine or autocrine loop and regulates neuronal functions, therefore, may play a protective role in the AD pathogenesis.

Original languageEnglish
Pages (from-to)565-571
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - 9 Sep 2011


  • Alzheimer's disease (AD)
  • Amyloid-β (Aβ)
  • CXCL8
  • Human neuron
  • Neuroprotection
  • Tumor necrosis factor-α (TNF-α)


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