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Neurol Genet. 2018 Nov 14;4(6):e278. doi: 10.1212/NXG.0000000000000278. eCollection 2018 Dec.

Anti-inflammatory effects of dietary vitamin D3 in patients with multiple sclerosis.

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School of Nutrition and Food Sciences (R.H., M.M), Tabriz University of Medical Sciences; Road Traffic Injury Research Center (M.A.-J), Tabriz University of Medical Sciences; Ardabil Province (D.A.); Department of Genetics (S.S.H.-A.), School of Medicine, Ardabil University of Medical Sciences; Department of Biochemistry and Diet Therapy (S.R.-A.), School of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Iran.



To assess the effects of dietary vitamin D3 on proinflammatory (interleukin-17A [IL-17A] and IL-6) and anti-inflammatory (IL-10) cytokines.


Our study was conducted on 75 participants who were divided into 3 groups: multiple sclerosis participants (MSPs, n = 25), first-degree relative participants (FDRPs, n = 25), and healthy participants (HPs, n = 25). All groups received 50,000 IU vitamin D3/wk for 8 weeks. Serum 25-(OH) vitamin D3 levels and messenger RNA (mRNA) expression levels of ILs were determined using electrochemiluminescence assay and real-time PCR, respectively.


Vitamin D3 affected the levels of IL-17A, IL-10, and IL-6 among the 3 groups (p < 0.001 for all). Levels of IL-17A (MSPs: fold change [FC] = 5.9, p = 0.014; FDRPs: FC = 5.2, p = 0.006; HPs: FC = 4.2, p = 0.012) and IL-6 (MSPs: FC = 5.6, p = 0.003; FDRPs: FC = 5.5, p = 0.002; HPs: FC = 5.1, p < 0.001) were downregulated after vitamin D3 treatment. In addition, levels of IL-10 (MSPs: FC = 6.2, p = 0.005; FDRPs: FC = 4.6, p < 0.001; HPs: FC = 5.2, p < 0.001) were upregulated after 8 weeks.


Although supplementation with vitamin D3 reduced the mRNA expression levels of IL-17A and IL-6, it increased the mRNA expression level of IL-10 in all groups. However, these effects were more considerable in the MSP group than in the other groups. Of interest, in a deficiency state of serum vitamin D3, IL-17A expression had a positive feedback effect on the expression of IL-6. Conversely, in the sufficient state, IL-10 expression had a negative feedback effect on the expression of IL-17A and IL-6.

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