Wei Hongen, Mori Susumu, Hua Kegang, Li Xiaohong
Central Laboratory, Shanxi Provincial People's Hospital, Taiyuan, China.
Int J Dev Neurosci. 2012 Nov;30(7):554-9. doi: 10.1016/j.ijdevneu.2012.08.007. Epub 2012 Aug 23.
Abnormal neuroimmune responses have been reported to be associated with autism and could be appropriate targets for pharmacologic intervention. Our previous studies showed that neuroimmune factor, interleukin (IL)-6, was significantly elevated in the fontal cortex and cerebellum of autistic subjects. The IL-6 overexpressing mice displayed several autism-like features as well as an abnormal dendritic spine morphology and synaptic function. The purpose of this study was to examine the volumetric differences in the brain of IL-6 overexpressing mice and compare with corresponding control mice using magnetic resonance imaging. Here we show that IL-6 overexpressing mice display an increase in the total brain volume. In addition, the lateral ventricle is also enlarged in the IL-6 overexpressing mice. The brain structures surrounding the lateral ventricle were squeezed and deformed from the normal location. These results indicate that IL-6 elevation in the brain could mediate neuroanatomical abnormalities. Taking together with our previous findings, a mechanism by which IL-6 may be involved in the pathogenesis of autism is proposed.
据报道,异常的神经免疫反应与自闭症有关,可能是药物干预的合适靶点。我们之前的研究表明,神经免疫因子白细胞介素(IL)-6在自闭症患者的额叶皮质和小脑中显著升高。过表达IL-6的小鼠表现出一些自闭症样特征以及异常的树突棘形态和突触功能。本研究的目的是使用磁共振成像检查过表达IL-6的小鼠大脑的体积差异,并与相应的对照小鼠进行比较。在这里,我们表明过表达IL-6的小鼠大脑总体积增加。此外,过表达IL-6的小鼠侧脑室也扩大。侧脑室周围的脑结构从正常位置被挤压并变形。这些结果表明,大脑中IL-6升高可能介导神经解剖学异常。结合我们之前的发现,提出了一种IL-6可能参与自闭症发病机制的机制。