Neuro-Behçet's Syndrome and Neuroinflammatory Molecules

Abstract

Neuro-Behçet's Syndrome and Neuroinflammatory Molecules Scientific background: In Neuro-Behçet's Syndrome (NBS) tumor necrosis factor-a (TNF-a) and interleukin 6 (IL-6) levels are found to be high in serum and cerebrospinal fluid (CSF) at active stage. An increase in IL-6 activates homocysteine, which in turn stimulates TNF-a. It is suggested that chemokines alsa play a part in N85 pathogenesis in addition to proinflammatory cytokines. Furthermore, it has been demonstrated that CXCL8 and CXCL10 increase in serum and CSF while any study on MIP-1· and RANTES could not be noted. Although there are some studies that show an increase in etiopathological molecules of Endothelin 1 (ET-1) and nitric oxide (NO) at the active stage in Behçet's Disease (BD), a corresponding study could not be found with respect to NBS. Objectives: The aim was to study the levels of TNF-a and IL-6 of neuroinflammatory mediators as well as those of MIP-1a, RANTES, which had never been studied before, and homocysteine, ET-1 and NO levels at active and inactive stages in comparison to control subjects so as to investigate the roles of the foregoing in the pathogenesis of Neuro-Behçet's syndrome. Material and methods: Levels of TNF-a, IL-6, MIP- 1a, RANTES, homocysteine, ET- 7 and NO2+NO3, i.e. a stable metabolite of NO, were investigated in 82 patients with NBS, in 196 BD patients without any neurological complications, and in 30 normal control subjects. Results: At the active stage, the TNF-a and IL-6 levels and the levels of MIP-1a, RANTES, which had not been studied before, and those of homocysteine, ET-1 and NO were found to be high when compared to inactive stage and the control subjects. Conclusions: it is suggested that the said immunoinflammatory molecules interact with each other and are involved in NBS pathogenesis; and therefore, target-specific immunotherapeutic methods will prove helpful in treatment.