白血病抑制因子是一种抗炎和镇痛细胞因子。
Leukemia inhibitory factor is an anti-inflammatory and analgesic cytokine.
作者信息
Banner L R, Patterson P H, Allchorne A, Poole S, Woolf C J
机构信息
Division of Biology, California Institute of Technology, Pasadena, California 91125, USA.
出版信息
J Neurosci. 1998 Jul 15;18(14):5456-62. doi: 10.1523/JNEUROSCI.18-14-05456.1998.
Abstract
The mRNA for leukemia inhibitory factor (LIF), a neuroimmune signaling molecule, is elevated during skin inflammation produced by intraplantar injection of complete Freund's adjuvant (CFA). Moreover, although LIF knock-out mice display normal sensitivity to cutaneous mechanical and thermal stimulation compared with wild-type mice, the degree of CFA-induced inflammation in mice lacking LIF is enhanced in spatial extent, amplitude, cellular infiltrate, and interleukin (IL)-1beta and nerve growth factor (NGF) expression. Conversely, local injection of low doses of recombinant LIF diminishes mechanical and thermal hypersensitivity as well as the IL-1beta and NGF expression induced by CFA. These data show that upregulation of LIF during peripheral inflammation serves a key, early anti-inflammatory role and that exogenous LIF can reduce inflammatory hyperalgesia.
摘要
白血病抑制因子（LIF）是一种神经免疫信号分子，其信使核糖核酸（mRNA）在通过足底注射完全弗氏佐剂（CFA）产生的皮肤炎症过程中水平升高。此外，尽管与野生型小鼠相比，LIF基因敲除小鼠对皮肤机械和热刺激表现出正常的敏感性，但缺乏LIF的小鼠中CFA诱导的炎症在空间范围、幅度、细胞浸润以及白细胞介素（IL）-1β和神经生长因子（NGF）表达方面均增强。相反，局部注射低剂量重组LIF可减轻CFA诱导的机械和热超敏反应以及IL-1β和NGF表达。这些数据表明，外周炎症期间LIF的上调发挥着关键的早期抗炎作用，并且外源性LIF可减轻炎症性痛觉过敏。
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