Toll-like receptor-4 expression in glial cells in mouse model of cuprizone-induced demyelination.

Objective: Multiple sclerosis (MS) is a T-cell mediated autoimmune central nervous system (CNS) disease. Although the etiopathogenetic factors of multiple sclerosis remain unclear, autoimmune mechanisms that associated with genetic predisposition and environmental triggers are suspected. Tolllike receptors (TLRs) mediate immune response to autologous components. It has been shown that microglia are the highest TLR4 expressing cell in the CNS. Several studies have shown that certain TLRs are over-expressed in MS. However, to our knowledge, the expression of TLR4 in cuprizone-induced demyelination has not been demonstrated previously. In the light of the information mentioned above, we aimed to evaluate the expression of TLR4 in glial cells in a mouse model of cuprizone-induced demyelination. Methods: In this study, we used the cuprizone model in mice to investigate the expression of TLR4. Forty male C57BL/6 type mice were used. Four groups were designed as demyelination/control and remyelination/control. 0,2% cuprizone was used to induce demyelination. TLR4 expressions in glial cells were evaluated with immunohistochemistry. Results: We show a significantly increased expression of TLR4 in the glial cells of the demyelination group. The expression of TLR4 was significantly higher in the demyelination group than the remyelination group. Besides, TLR4 expression in demyelinated mice glial cells was higher than the control groups. Conclusion: We showed that TLR4 expressions were significantly higher in demyelinated mice. High expressions of TLR4 may indicate that it could be one of the underlying mechanisms of immune activation in MS. We believe that histopathological and molecular studies are necessary to obtain further information on the background of the disease. [ABSTRACT FROM AUTHOR]