Visfatin/NAMPT/PBCEF and Cytokine Concentration in Multiple Sclerosis Patients Compared to Healthy Subjects

Abstract

The aim of the study is to measure IL-1 β, TNF-α, hs-CRP levels and Nampt/visfatin/PBCEF concentrations in patients with multiple sclerosis and to compare them with those of healthy control subjects. In a case-control study a total number of 192 people were recruited. Ninety-six of them were suffering from multiple sclerosis, age 34.80±8.75 years (mean±SD), who were referred form the Iranian Multiple Sclerosis Society. They included relapsing remitting (82 subjects) and both primary and secondary progressive (14 subjects) types of MS. The diagnosis was made according to the diagnostic criteria by a neurology consultant. Ninety-six healthy individuals were recruited from the Iranian Multicenter Osteoporosis Study (IMOS) as the control group. Following an overnight fasting, peripheral blood was taken from all subjects and centrifuged in order to separate serum for measurement of serum visfatin, Interleukin-1beta (IL-1β), TNF-α, and hs-CRP concentrations. Fat tissue mass was measured using DXA. Levels of visfatin, TNF-α and hs-CRP were significantly higher in MS patients. Besides, significant correlation was found between visfatin levels and those of TNF-α, IL-1β, hs-CRP in MS patients. Regarding the control group, significant correlation was found between visfatin levels and levels of TNF-α. However, we did not find any significant correlation between fat tissue mass and visfatin, TNF-α, IL-1β or hs-CRP levels in the MS group. However, there was a significant correlation between fat tissue mass and TNF-α level in the study population. Our findings demonstrated that proinflammatory factor levels were, although not significantly, higher in RRMS patients compared to PPMS and SPMS patients. The results suggest that levels of visfatin and pro-inflammatory cytokines are higher in MS patients compared to healthy subjects. Their higher levels may be, in part, attributable to the MS phenotypes independent of fat mass in patients. We believe that these results may shed some light on a potentially novel source of visfatin as well as explaining its regulating role in the inflammation process.