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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >1,25-dihydroxyvitamin D3 treatment decreases macrophage accumulation in the CNS of mice with experimental autoimmune encephalomyelitis.
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1,25-dihydroxyvitamin D3 treatment decreases macrophage accumulation in the CNS of mice with experimental autoimmune encephalomyelitis.

机译：1,25-二羟基维生素D3处理可降低实验性自身免疫性脑脊髓炎小鼠中巨噬细胞的蓄积。

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摘要

Sunlight, which is required for vitamin D biosynthesis, may be protective in multiple sclerosis (MS), due to the immunoregulatory functions of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), the hormonally active vitamin D metabolite. This hypothesis provided the impetus for the experiments reported here investigating mechanisms whereby 1,25-(OH)2D3 may inhibit murine experimental autoimmune encephalomyelitis (EAE). Severe EAE was induced, 1,25-(OH)2D3 or mock treatment was administered, and clinical disease, histopathological disease, and encephalitogenic cells in the central nervous system (CNS) were analyzed within 24-72 h of the treatment. The mock-treated mice remained paralyzed (stage 3 EAE) while most hormone-treated animals regained the partial use of both hind limbs (stage 2 EAE) within 72 h of treatment. A histopathological examination showed the hormone-treated mice had a 50% decrease in white matter and meningeal inflammation at 72 h post treatment. A flow cytometric analysis of cell surface markers on spinal cord cells recovered 24 h post treatment showed the mock-treated mice with EAE had about 7.0 +/- 2.3 million Mac-1+ cells/cord, whereas the hormone-treated mice had about 2.1 +/- 2.6 million Mac-1+ cells/cord, which was not significantly different from the unmanipulated control mice. Otherwise, the flow cytometric analysis detected no significant differences between the groups with respect to CD4+ or CD8+ T cells or B cells or macrophages in draining lymph nodes or spinal cords. These results are discussed with regard to possible fates for the 5 million Mac-1+ cells that were rapidly lost from the inflamed CNS in the 1,25-(OH)2D3-treated mice, and the possible beneficial effect of hormone treatment in resolving acute MS.
机译：维生素D生物合成所需的阳光在多发性硬化症（MS）中可能具有保护作用，这是由于1,25-二羟基维生素D3（1,25-（OH）2D3）（一种具有激素活性的维生素D代谢产物）的免疫调节功能。该假设为此处报道的研究机制提供了动力，其中1,25-（OH）2D3可以抑制鼠类实验性自身免疫性脑脊髓炎（EAE）。诱发严重的EAE，给予1,25-（OH）2D3或模拟治疗，并在治疗的24-72小时内分析临床疾病，组织病理学疾病和中枢神经系统（CNS）的致脑细胞。模拟治疗的小鼠仍处于瘫痪状态（EAE 3期），而大多数激素治疗的动物在治疗72小时内恢复了部分后肢的局部使用（EAE 2期）。组织病理学检查显示，用激素治疗的小鼠在治疗后72小时白质和脑膜发炎减少了50％。用流式细胞仪分析处理后24小时恢复的脊髓细胞的细胞表面标志物，结果显示，用EAE模拟处理的小鼠约有7.0 +/- 230万Mac-1 +细胞/帘线，而用激素处理的小鼠约有2.1 +/- 260万个Mac-1 +细胞/帘线，与未操纵的对照小鼠没有显着差异。否则，流式细胞仪分析检测到两组之间在引流淋巴结或脊髓中的CD4 +或CD8 + T细胞或B细胞或巨噬细胞方面无显着差异。这些结果讨论了在1,25-（OH）2D3处理的小鼠中因发炎的中枢神经系统而迅速失去的500万Mac-1 +细胞的可能命运以及激素治疗在解决中的潜在有益作用急性MS。

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