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IL-8 enhancement of amyloid-beta (Abeta 1-42)-induced expression and production of pro-inflammatory cytokines and COX-2 in cultured human microglia.

Franciosi, S | Choi, HB | Kim, SU  | McLarnon, JG
Journal of neuroimmunology, 159(1-2). : 66-74, 2005
Journal Title
Journal of neuroimmunology
The effects of the chemokine IL-8 on amyloid beta peptide (Abeta(1-42))-induced responses in cultured human microglia were investigated using RT-PCR, ELISA and immunocytochemistry. Abeta(1-42) (5 microM) applied for 8 h induced the expression and increased the production of the pro-inflammatory cytokines IL-6, IL-1beta, TNF-alpha, the inducible enzyme COX-2 and chemokine IL-8. Microglial treatment with IL-8 added (at 100 ng/mL) with Abeta(1-42) led to enhancement in both expression and production of all of these pro-inflammatory factors compared with peptide alone. Stimulation with IL-8 itself was effective in increasing microglial expression of pro-inflammatory cytokines, IL-8 and COX-2, however, had no effect on protein levels of all these factors. The expression of the anti-inflammatory cytokines IL-10 and TGFbeta(1) remained unchanged from basal levels with stimulation using either Abeta(1-42), IL-8 or the peptide together with IL-8. The actions of IL-8 to potentiate Abeta(1-42)-induced inflammatory mediators may have particular relevance to Alzheimer disease brain which exhibits elevated levels of the chemokine.

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Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
Ajou Authors
김, 승업
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