Expression of TNFα in central neurons of Lewis rat spinal cord after EAE induction

✍ Scribed by Henri Villarroya; Yannick Marie; Jean-Christophe Ouallet; Françoise Le Saux; Jean-Léon Tchélingérian; Nicole Baumann

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 523 KB
• Volume: 49
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/(sici)1097-4547(19970901)49:5<592::aid-jnr9>3.0.co;2-6

✦ Synopsis

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␣, 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␣ in spinal cord of Lewis rats, during the critical phase of EAE. The expression of TNF␣ 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␣-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␣ cytokine. In addition, neuronal-TNF␣ detection in the recovery stage of EAE may suggest a role other than its classical action in promoting inflammatory processes.