Villarroya H, Marie Y, Ouallet J C, Le Saux F, Tchélingérian J L, Baumann N
INSERM U 134, Hôpital de la Salpêtrière, Paris, France.
J Neurosci Res. 1997 Sep 1;49(5):592-9. doi: 10.1002/(SICI)1097-4547(19970901)49:5<592::AID-JNR9>3.0.CO;2-6.
Experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis (MS), is a demyelinating autoimmune disease of the central nervous system (CNS). The proinflammatory cytokine TNF alpha, as an endogenous mediator of inflammation, plays an important role in the pathogenesis of EAE disease. In this study, we demonstrate the presence of TNF alpha in spinal cord of Lewis rats, during the critical phase of EAE. The expression of TNF alpha is observed mainly in the gray matter of thoracic and lumbar levels of the spinal cord, in the motoneurons and interneurons of the ventral horn. Surprisingly, one month after recovery, we still found an intense TNF alpha-neuronal expression, including in the cervical region, and this positivity lasted up to 40 days after recovery, with, however, a decrease in its intensity. These results suggest that central neurons respond directly to massive infiltration of lymphocytes and macrophages after the breakdown of the blood-brain barrier (BBB), by producing TNF alpha cytokine. In addition, neuronal-TNF alpha detection in the recovery stage of EAE may suggest a role other than its classical action in promoting inflammatory processes.
实验性自身免疫性脑脊髓炎（EAE）是多发性硬化症（MS）的动物模型，是一种中枢神经系统（CNS）的脱髓鞘自身免疫性疾病。促炎细胞因子肿瘤坏死因子α（TNFα）作为炎症的内源性介质，在EAE疾病的发病机制中起重要作用。在本研究中，我们证明了在EAE的关键阶段，Lewis大鼠脊髓中存在TNFα。TNFα的表达主要在脊髓胸段和腰段的灰质中观察到，位于腹角的运动神经元和中间神经元中。令人惊讶的是，恢复一个月后，我们仍然发现强烈的TNFα神经元表达，包括在颈部区域，并且这种阳性在恢复后持续长达40天，然而其强度有所下降。这些结果表明，在血脑屏障（BBB）破坏后，中枢神经元通过产生TNFα细胞因子直接对淋巴细胞和巨噬细胞的大量浸润作出反应。此外，在EAE恢复阶段检测到神经元TNFα可能表明其在促进炎症过程中的经典作用之外还有其他作用。
