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Expression of TNFα in central neurons of Lewis rat spinal cord after EAE induction
Author(s) -
Villarroya Henri,
Marie Yannick,
Ouallet JeanChristophe,
Saux Françoise Le,
Tchélingérian JeanLéon,
Baumann Nicole
Publication year - 1997
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19970901)49:5<592::aid-jnr9>3.0.co;2-6
Subject(s) - experimental autoimmune encephalomyelitis , spinal cord , multiple sclerosis , central nervous system , tumor necrosis factor alpha , cytokine , proinflammatory cytokine , medicine , neuroscience , encephalomyelitis , inflammation , immunology , pathogenesis , biology
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 TNFα, as an endogenous mediator of inflammation, plays an important role in the pathogenesis of EAE disease. In this study, we demonstrate the presence of TNFα in spinal cord of Lewis rats, during the critical phase of EAE. The expression of TNFα 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 TNFα‐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 TNFα cytokine. In addition, neuronal‐TNFα detection in the recovery stage of EAE may suggest a role other than its classical action in promoting inflammatory processes. J. Neurosci. Res. 49:592–599, 1997. © 1997 Wiley‐Liss, Inc.