Akagi Takanori, Matsumura Yuta, Yasui Masaya, Minami Emiko, Inoue Hidemasa, Masuda Takahiro, Tozaki-Saitoh Hidetoshi, Tamura Tomohiko, Mizumura Kazue, Tsuda Makoto, Kiyama Hiroshi, Inoue Kazuhide
Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan.
J Pharmacol Sci. 2014;126(2):172-6. doi: 10.1254/jphs.14143sc. Epub 2014 Oct 2.
We investigated the role of interferon regulatory factor 8 (IRF8) in a model of chronic pain in which repeated cold stress (RCS) exposure produces tactile allodynia. RCS exposure produced a decrease in paw withdrawal threshold (PWT) to mechanical stimulation. Spinal microglia of RCS-exposed mice were morphologically activated. Expression of IRF8 was significantly increased in the spinal cord of RCS-exposed mice and was localized in microglia. IRF8-knockout mice failed to show the RCS-induced decrease in PWT. Thus, RCS exposure activates spinal microglia and upregulation of IRF8 in these cells is involved in the development of tactile allodynia after RCS exposure.
我们研究了干扰素调节因子8(IRF8)在慢性疼痛模型中的作用,在该模型中,反复冷应激(RCS)暴露会产生触觉异常性疼痛。RCS暴露导致对机械刺激的爪退缩阈值(PWT)降低。暴露于RCS的小鼠脊髓小胶质细胞在形态上被激活。暴露于RCS的小鼠脊髓中IRF8的表达显著增加,且定位于小胶质细胞。IRF8基因敲除小鼠未表现出RCS诱导的PWT降低。因此,RCS暴露会激活脊髓小胶质细胞,这些细胞中IRF8的上调参与了RCS暴露后触觉异常性疼痛的发展。