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.