把多发性硬化(MS)和维生素D分开

2010-03-23 00:00 · Lisa

科学家发现紫外线辐射可能抑制多发性硬化(MS),而且独立于维生素D的制造,这个结果与长久以来的一个假说相矛盾,即由阳光照射增加的维生素D浓度降低了MS的发病率。这一假说是建立在一种观察的结果上,即MS很少见于赤道附近的人群,而且更常见于极地附近的人群。Hector DeLuca及

科学家发现紫外线辐射可能抑制多发性硬化(MS),而且独立于维生素D的制造,这个结果与长久以来的一个假说相矛盾,即由阳光照射增加的维生素D浓度降低了MS的发病率。这一假说是建立在一种观察的结果上,即MS很少见于赤道附近的人群,而且更常见于极地附近的人群。Hector DeLuca及其同事研究了患有一种实验性多发性硬化症的小鼠持续暴露在紫外线下对维生素D制造的影响,结果发现接触常规紫外线辐射的小鼠(这是为了模拟在赤道附近的生活)比对照组的MS症状更轻。这组科学家让另一组小鼠服用维生素补充剂,从而达到紫外线自然产生的维生素的水平,但是没有进行紫外线照射。这组小鼠没有表现出MS发病率或严重程度的减少,这提示如果紫外线辐射通过某种其他路径减少了MS症状,补充维生素D可能不会代替阳光减少MS易感性的能力。

论文 #10-01119: “Ultraviolet radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production,” 作者 Bryan R. Becklund, Kyle S. Severson, Souriya V. Vang和Hector F. DeLuca

媒体联系人:Hector DeLuca,威斯康星大学麦迪逊分校生物化学系

Department of Biochemistry, University of Wisconsin, Madison, WI

电话:608-262-1620

电子邮件:deluca@biochem.wisc.edu

Published online before print March 22, 2010, doi: 10.1073/pnas.1001119107

UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production

Bryan R. Becklund, Kyle S. Severson, Souriya V. Vang, and Hector F. DeLuca1

Abstract

Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D3 [25(OH)D3] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1α,25-dihydroxyvitamin D3, suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D3 and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D3 levels. Further analysis demonstrated that the levels of 25(OH)D3 obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility.

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