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To identify serum cytokine networks specific to chronic inflammatory demyelinating polyneuropathy (CIDP), serum samples of two subgroups (18 patients with typical CIDP and 12 patients with multifocal acquired demyelinating sensory and motor neuropathy [MADSAM]) were analyzed with multiplex magnetic bead-based cytokine assay. TNF-α, HGF, MIP-1β and IL-1β levels were significantly higher in total CIDP patients than in normal controls. Of these, HGF levels were elevated in typical CIDP patients, but not in MADSAM patients. Patients with high HGF levels showed good responses to steroid treatment. Different cytokine profiles among the CIDP subtypes presumably reflect differences in pathophysiology., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Of 37 multiple sclerosis patients, 19 suboptimal responders were randomized to 375 (n=12) or 250µg (n=7) interferon (IFN)-β-1b. mRNA levels of 23 cytokines, chemokines, and chemokine receptors were quantified by TaqMan low-density array (TLDA) real-time polymerase chain reaction. Better treatment responses or increased IFN-β doses were associated with elevated IL-10 and TGF-β and decreased CXCL10, IL-18, IFN-γ, and TNF-α transcript levels. Adjusting for dose, poor treatment responses resulted in a 4-fold increase in CXCL10 and IFN-γ expression (Mantel-Haenszel RR=3.74, p<0.0001). CXCL10 and IFN-γ mRNA levels were reliable indicators of treatment response. TLDA can be used to tailor IFN-β-1b therapy., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Dysregulation in the expression of pro- and anti-inflammatory cytokines is one of the milestones in multiple sclerosis (MS) development and progression. The aim of this study was to investigate the possible influence of TNF-alpha (-308), TGF-beta (codons 10 and 25), IL-10 (-1082, -819, -592), IL-6 (-174) and IFN-gamma (+874) polymorphisms on susceptibility to multiple sclerosis (MS). Genotyping was performed by PCR-SSP method in 55 MS patients with relapsing-remitting form of the disease and 86 healthy subjects from Bulgarian population. We observed a statistically significant increase in the CC genotype of IL-10 -819 and -592 SNPs coupled with a decreased frequency of the TGF-beta +915 CG genotype in our MS patients (Pc<0.05). No significant differences were observed between MS patients and controls with respect to the distribution of the other cytokine gene polymorphisms investigated. Although the size of the study group is small, these results indicate that polymorphic variations of two of the major anti-inflammatory cytokines, IL-10 and TGF-beta, may play a role in MS susceptibility.

We assessed the action of mitoxantrone (MX) when given as rescue therapy in patients with relapsing-remitting (RR) multiple sclerosis (MS), whose disease activity worsens despite IFN-beta treatment. Ten very active RR MS patients received MX 12 mg/m2 monthly, for 3 months, and then returned to the original treatment with IFN-beta. Following treatment with MX, 70% of patients were able to return to IFN-beta treatment, stabilising EDSS and relapse rate during a follow-up period of 15-18 additional months. In contrast, in 30% of the patients who were taken off MX and returned to IFN-beta treatment the EDSS score deteriorated and the number of exacerbations increased significantly. The latter patients were switched again to MX treatment at 3-month intervals, stabilising EDSS and relapse rate during 15-18 additional months. Clinical findings correlated with the number of Gd-enhancing lesions disclosed in MRI scans. Immunological data were consistent with the clinical and MRI benefits observed. We conclude that brief courses of MX may provide a safe treatment alternative for RR MS patients who experience rapid and severe worsening of their disease despite IFN-beta treatment.