CX3CR1型
小胶质细胞
神经保护
趋化因子
CX3CL1型
神经毒性
中枢神经系统
肿瘤坏死因子α
星形胶质细胞
生物
细胞生物学
免疫学
神经科学
趋化因子受体
炎症
医学
内科学
毒性
作者
Tetsuya Mizuno,Jun Koyama,Kenji Numata,Akio Suzumura
出处
期刊:Brain Research
[Elsevier]
日期:2003-07-01
卷期号:979 (1-2): 65-70
被引量:298
标识
DOI:10.1016/s0006-8993(03)02867-1
摘要
The CX3C-chemokine, fractalkine is reportedly to be expressed in the central nervous system, and up-regulated in certain pathological conditions, such as HIV encephalopathy and multiple sclerosis. In the present study, we examined the production of fractalkine and the expression of its receptor, CX3CR1 in murine glial and neuronal cell in vitro, and investigated its neuroprotective functions. Both fractalkine and CX3CR1 were expressed constitutively in neurons, microglia, and astrocytes. Neither the production of fractalkine nor its receptor expression was up-regulated by lipopolysaccharide (LPS), as measured by mRNA expression and protein synthesis. Fractalkine dose-dependently suppressed the production of nitric oxide (NO), interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha with activated microglia. It also significantly suppressed neuronal cell death induced by microglia activated with LPS and interferon-gamma, in a dose-dependent manner. These results suggest the possible functions of fractalkine as an intrinsic inhibitor against neurotoxicity by activated microglia.
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