Staphylococcus aureus induces microglial inflammation via a glycogen synthase kinase 3β-regulated pathway

Yi Lin Cheng, Chi Yun Wang, Wei Ching Huang, Cheng Chieh Tsai, Chia Ling Chen, Ching Fen Shen, A. Yu Chi, Chiou Feng Lin

研究成果: Article同行評審

38 引文 斯高帕斯(Scopus)

摘要

A proinflammatory role for glycogen synthase kinase 3β (GSK-3β) has been demonstrated. Here, we addressed its roles on heat-inactivated Staphylococcus aureus-induced microglial inflammation. Heat-inactivated S. aureus induced tumor necrosis factor alpha (TNF-α) and nitric oxide (NO) production, at least in part, via a Toll-like receptor 2-regulated pathway. Neutralization of TNF-α largely blocked heat-inactivated S. aureus-induced NO. Heat-inactivated S. aureus activated GSK-3β, and inhibiting GSK-3β reduced TNF-α production as well as inducible NO synthase (iNOS)/NO biosynthesis. While activation of NF-κB was essential for heat-inactivated S. aureus-induced TNF-α and NO, inhibiting GSK-3β blocked heat-inactivated S. aureus-induced NF-κB p65 nuclear translocation. Additionally, inhibiting GSK-3β enhanced heat-inactivated S. aureus-induced interleukin-10 (IL-10) production (IL-10 is an anti-inflammatory cytokine which inhibits TNF-α production). Neutralization of IL-10 reduced TNF-α downregulation caused by GSK-3β inhibition. These results suggest that GSK-3β regulates heat-inactivated S. aureus-induced TNF-α and NO production in microglia mainly by activating NF-κB and probably by inhibiting IL-10.

原文English
頁(從 - 到)4002-4008
頁數7
期刊Infection and Immunity
77
發行號9
DOIs
出版狀態Published - 2009 九月

All Science Journal Classification (ASJC) codes

  • 寄生物學
  • 微生物學
  • 免疫學
  • 傳染性疾病

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