Changes in serum cytokine profile and deficit severity in patients with relapsing-remitting multiple sclerosis

Abstract

Introduction: In experimental autoimmune encephalomyelitis, neurological deficit correlates with axonal loss and the CD8+ T cells are a likely mediator of axonal damage. In relapsing-remitting multiple sclerosis, there is a correlation of the immune inflammatory activity in the lesion foci with the axon transection. Aim: To evaluate the changes occurring in the serum concentrations of TNF-α, IFN-γ, IL17, TGF-β1, IL4, and IL10 during relapse and remission, and their correlations with the degree of neurological deficit. Materials and methods: In an open, prospective, case-control study conducted between 2012 and 2014, we examined 86 people: 46 patients (33 women and 13 men) and 40 healthy individuals (20 women and 20 men). Serum cytokine concentrations were analyzed using ELISA – once in the controls, twice in the patients during the relapse and remission of the condition. The collected data were analyzed using SPSS 19.0. We used the Kolmogorov-Smirnov test, the independent sample t-test, the Spearman and Pearson correlation, the Mann-Whitney test, and regression analysis. Results: Immune imbalance was found in the patients compared to the healthy controls in both relapse and remission. During the relapse, the IFN-γ levels were significantly increased compared to the levels in remission (p=0.017). During remission, the deficit was statistically significantly improved (p<0.001) and the anti-inflammatory IL4 and TGF-β1 were increased compared to their levels in the exacerbation period (p=0.006 and p=0.009, respectively). There was a causal relationship between the serum concentrations of TNF-α and EDSS in relapse (Vanetto-significance). During this phase, the regression analysis established two factors that had statistically significant influence on the deficit severity – TNF-α and IL17 (t=2.093, p=0.042; t=−2.140, p=0.038). Conclusions: IL17 and TNF-α serum concentrations are significant factors for the neurological deficit severity. The levels of IFN-γ, IL4, and TGF-β1 during both periods are criteria for evaluation of the immune inflammatory activity.