Kurkowska-Jastrzebska I, Bałkowiec-Iskra E, Ciesielska A, Joniec I, Cudna A, Zaremba M M, Członkowski A, Członkowska A
2nd Department of Neurology, Institute of Psychiatry and Neurology, Sobieskiego 9, Warsaw, Poland.
Int Immunopharmacol. 2009 Jun;9(6):781-91. doi: 10.1016/j.intimp.2009.03.003. Epub 2009 Mar 13.
The response of the immune system during injury of the central nervous system may play a role in protecting neurons. We have previously reported that immunization with MOG 35-55 prior to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced injury of the dopaminergic system promotes less dopamine depletion and less dopaminergic damage of neurons in mice. In this study, we evaluate the influence of MOG immunization on the inflammatory reaction that occurs at the place of injury. C57Bl male mice, 2 and 12 months old, received i.p. injections of MPTP (40 mg/kg) and some groups animals also received an additional injection with myelin oligodendrocyte glycoprotein (MOG) 35-55 in CFA 6 days before MPTP administration. MPTP caused a common inflammatory reaction characterized by microglial activation, infiltration of T cells into the substantia nigra and striatum and increased expression of mRNA encoding pro-inflammatory cytokines (IL-1 beta, TNFalpha, INF gamma) and trophic factors (TGFbeta, GDNF). MOG immunization prior to MPTP administration significantly diminished the microglial reaction and reduced the levels of infiltrating CD8+ lymphocytes. The number of CD4+ T cells remained at the same level as in the MPTP group. Expression of pro-inflammatory cytokines was diminished. The mRNA expression of GDNF was significantly higher in the MOG pretreated mice relative to the MPTP group, both in the 2 month old and 12 month old groups. Since MOG immunization prior to MPTP intoxication appears to prevent nigrostriatal injury, the observed decrease of inflammation and increase of GDNF mRNA expression in the injured areas might represent one of the mechanisms of observed neuroprotection.
中枢神经系统损伤期间免疫系统的反应可能在保护神经元方面发挥作用。我们之前曾报道,在1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的多巴胺能系统损伤之前用髓鞘少突胶质细胞糖蛋白(MOG)35-55进行免疫接种,可使小鼠体内多巴胺耗竭减少,神经元的多巴胺能损伤减轻。在本研究中,我们评估了MOG免疫接种对损伤部位发生的炎症反应的影响。2个月和12个月大的C57Bl雄性小鼠腹腔注射MPTP(40 mg/kg),部分组的动物在给予MPTP前6天还额外注射了CFA中的髓鞘少突胶质细胞糖蛋白(MOG)35-55。MPTP引发了一种常见的炎症反应,其特征为小胶质细胞活化、T细胞浸润到黑质和纹状体以及编码促炎细胞因子(IL-1β、TNFα、INFγ)和营养因子(TGFβ、GDNF)的mRNA表达增加。在给予MPTP之前进行MOG免疫接种可显著减轻小胶质细胞反应,并降低浸润的CD8 +淋巴细胞水平。CD4 + T细胞数量与MPTP组保持在同一水平。促炎细胞因子的表达减少。在2个月龄和12个月龄组中,相对于MPTP组,MOG预处理小鼠中GDNF的mRNA表达均显著更高。由于在MPTP中毒之前进行MOG免疫接种似乎可预防黑质纹状体损伤,因此在损伤区域观察到的炎症减少和GDNF mRNA表达增加可能是观察到的神经保护机制之一。