4.3 Article

Interleukin-10 inhibits endotoxin-induced pro-inflammatory cytokines in microglial cell cultures

期刊

JOURNAL OF NEUROIMMUNOLOGY
卷 162, 期 1-2, 页码 71-80

出版社

ELSEVIER
DOI: 10.1016/j.jneuroim.2005.01.010

关键词

microglia; inflammation; cytokine

资金

  1. NICHD NIH HHS [HD30704-09] Funding Source: Medline

向作者/读者索取更多资源

Inflammation contributes to perinatal brain injury and can be induced by hypoxia-ischemia (HI) or exposure to infection (fetal inflammatory response). The anti-inflammatory cytokine interleukin-10 (IL10) has been shown to have neuroprotective effects following HI. To determine whether IL10 can reduce the inflammatory response to lipopolysaccharide (LPS) in microglial cell cultures, primary microglial (MG) and/or HAPI cells (new MG-like cell line) were treated with LPS (50 ng/ml) in the presence or absence of IL10 (20 ng/ml) for 0.5, 1, 4, and 8 h. TNF alpha, MIP-1 alpha, and RANTES were assayed by ELISA. Chemokine receptors, CCR5, CXCR3, and CX3CR1 (fractalkine receptor) were assayed by semiquantitative RT-PCR. We found that in MG cell cultures TNF alpha, MIP-1 alpha, and RANTES release after 8-h exposure to LPS was significantly higher compared to non-exposed MG cells (P<0.001). In HAPI cell cultures similar stimulation of mRNA levels was found for TNF alpha, MIP-1 alpha, CXCR3, and CX(3)CR1. IL10 inhibited TNF alpha, MIP-1 alpha, and RANTES release of LPS-stimulated MG cells as well as TNF alpha MIP-1 alpha, and CXCR3 mRNA expression by HAPI cells after exposure to LPS (P<0.05). In contrast to those inhibitory effects, there was no change in fractalkine, and a modest increase in CX3CR1 mRNA levels was found in the presence of IL10. We conclude that the inflammatory response induced in microglial cells by LPS can be markedly reduced by IL10. The increase in fractalkine receptor (CX3CR1) is also potentially protective. Our results suggest that treatment of damaging neuroinflammatory insults such hypoxia-ischemia, with IL10 may be protective for the immature brain. (C) 2005 Elsevier B.V All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.3
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据