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Vitamine D remt ontstekingen*
Uit een laboratoriumstudie blijkt dat vitamine D op celniveau ontstekingsreacties doet verminderen en daardoor sterk ontstekingsremmend werkt. Doch dit gebeurt alleen als de bloedwaarden vitamine D hoog genoeg zijn. Vanaf 30 ng/ml begon vitamine D zijn werk te doen. Het meest effectief was vitamine D in het bestrijden van ontstekingen bij bloedwaarden van 50 ng/ml. Volgens de onderzoekers hebben mensen met chronische ontstekingsziektes zoals astma en artritis dus baat bij het nemen van supplementen van vitamine D om goede bloedwaarden vitamine D te krijgen.
Vitamin D Inhibits Monocyte/Macrophage Proinflammatory Cytokine Production by Targeting MAPK Phosphatase-1 
1. Yong Zhang*, 2. Donald Y. M. Leung*,†, 3. Brittany N. Richers*, 4. Yusen Liu‡§, 5. Linda K. Remigio*, 6. David W. Riches* and 
7. Elena Goleva*
+ Author Affiliations
1. *Department of Pediatrics, National Jewish Health, Denver, CO 80206; 
2. †Department of Pediatrics, University of Colorado Denver, Aurora, CO 80045; and
3. ‡Center for Perinatal Research, Research Institute at Nationwide Children’s Hospital, Columbus, OH 43205; 
4. §Department of Pediatrics, Ohio State University College of Medicine, Columbus, OH 43205 
1. Address correspondence and reprint requests to Dr. Elena Goleva, National Jewish Health, 1400 Jackson Street, Room K1016A, Denver, CO 80206. E-mail address: golevae@njhealth.org
Abstract
It is estimated that 1 billion people around the world are vitamin D deficient. Vitamin D deficiency has been linked to various inflammatory diseases. However, the mechanism by which vitamin D reduces inflammation remains poorly understood. In this study, we investigated the inhibitory effects of physiologic levels of vitamin D on LPS-stimulated inflammatory response in human blood monocytes and explored potential mechanisms of vitamin D action. We observed that two forms of the vitamin D, 1,25(OH)2D3, and 25(OH)D3, dose dependently inhibited LPS-induced p38 phosphorylation at physiologic concentrations, IL-6 and TNF-α production by human monocytes. Upon vitamin D treatment, the expression of MAPK phosphatase-1 (MKP-1) was significantly upregulated in human monocytes and murine bone marrow-derived macrophages (BMM). Increased binding of the vitamin D receptor and increased histone H4 acetylation at the identified vitamin D response element of the murine and human MKP-1 promoters were demonstrated. Moreover, in BMM from MKP1−/− mice, the inhibition of LPS-induced p38 phosphorylation by vitamin D was completely abolished. Vitamin D inhibition of LPS-induced IL-6 and TNF-α production by BMM from MKP-1−/− mice was significantly reduced as compared with wild-type mice. In conclusion, this study identified the upregulation of MKP-1 by vitamin D as a novel pathway by which vitamin D inhibits LPS-induced p38 activation and cytokine production in monocytes/macrophages. (Maart 2012)