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演題詳細

Oral

神経炎症と炎症性神経疾患
Neuroinflammation and Inflammatory Disease in Nervous System

開催日 2014/9/13
時間 15:00 - 16:00
会場 Room I(311+312)
Chairperson(s) 吉良 潤一 / Jun-ichi Kira (九州大学大学院医学研究院 神経内科学 / Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyusyu University, Japan)
錫村 明生 / Akio Suzumura (名古屋大学環境医学研究所 神経免疫 / Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Japan)

中枢神経系におけるinterleukin-19の役割
The role of interleukin-19 in the central nervous system

  • O3-I-3-1
  • 堀内 浩 / Hiroshi Horiuchi:1 竹内 英之 / Hideyuki Takeuchi:1 水野 哲也 / Tetsuya Mizuno:1 錫村 明生 / Akio Suzumura:1 
  • 1:名古屋大学 / Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Japan 

The role of interleukin-19 in the central nervous system
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University
Hiroshi HORIUCHI, Hideyuki TAKEUCHI, Tetsuya MIZUNO, Akio SUZUMURA

Purpose: Activated microglia has been considered to play a pivotal role in pathogenesis of a variety of neurologic disorders. We recently identified interleukin-19 (IL-19) as a markedly upregulated gene in activated microglia. In this study, we investigated the precise function of IL-19 in the central nervous system (CNS), which is still uncertain.
Methods: Protocols for animal experiments were approved by the Animal Experiment Committee of Nagoya University. Mouse primary neurons, astrocytes, and microglia were prepared from C57BL6 embryos. The expression levels of IL-19 and its receptors were evaluated by quantitative PCR, Western blotting, or ELISAs. APP/PS1 Tg mice and SOD1 G93A Tg mice were used as an Alzheimer's disease model or an amyotrophic lateral sclerosis model, respectively.
Results: We found that microglia exclusively express the receptors for IL-19 in the CNS. Il-19 and its receptors were upregulated in microglia upon activation. IL-19 significantly suppressed the expression of mRNA and protein level of IL-6 and TNF-α in activated microglia. APP/PS1 Tg mice and SOD1 G93A Tg mice showed upregulation of IL-19 in the lesion associated with the disease progression.
Conclusion: We identified IL-19 as a novel anti-inflammatory cytokine from activated microglia. IL-19 may work as a self-limiter of neuroinflammation in various neurologic diseases.

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