Expression of TNF alpha in central neurons of Lewis rat spinal cord after EAE induction.

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.