紫外线对实验性自身免疫性脑脊髓炎的抑制作用并非由尿刊酸的异构化介导。
Suppression of experimental autoimmune encephalomyelitis by ultraviolet light is not mediated by isomerization of urocanic acid.
作者信息
Irving Amy A, Marling Steven J, Plum Lori A, DeLuca Hector F
机构信息
Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI, 53706, USA.
出版信息
BMC Neurosci. 2017 Jan 5;18(1):8. doi: 10.1186/s12868-016-0323-2.
BACKGROUND
Ultraviolet B irradiation confers strong resistance against experimental autoimmune encephalomyelitis, a model of multiple sclerosis. This protection by ultraviolet B is independent of vitamin D production but causes isomerization of urocanic acid, a naturally occurring immunosuppressant.
METHODS
To determine whether UCA isomerization from trans to cis is responsible for the protection against experimental autoimmune encephalomyelitis afforded by ultraviolet B, trans- or cis-urocanic acid was administered to animals and their disease progression was monitored.
RESULTS
Disease incidence was reduced by 74% in animals exposed to ultraviolet B, and skin cis-urocanic acid levels increased greater than 30%. However, increasing skin cis-urocanic acid levels independent of ultraviolet B was unable to alter disease onset or progression.
CONCLUSIONS
It is unlikely that urocanic acid isomerization is responsible for the ultraviolet B-mediated suppression of experimental autoimmune encephalomyelitis. Additional work is needed to investigate alternative mechanisms by which UVB suppresses disease.
背景
紫外线B照射可赋予针对实验性自身免疫性脑脊髓炎（一种多发性硬化症模型）的强大抵抗力。紫外线B的这种保护作用独立于维生素D的产生，但会导致尿刊酸（一种天然存在的免疫抑制剂）发生异构化。
方法
为了确定尿刊酸从反式到顺式的异构化是否是紫外线B对实验性自身免疫性脑脊髓炎提供保护的原因，将反式或顺式尿刊酸给予动物，并监测其疾病进展。
结果
暴露于紫外线B的动物疾病发病率降低了74%，皮肤顺式尿刊酸水平增加超过30%。然而，独立于紫外线B增加皮肤顺式尿刊酸水平并不能改变疾病的发作或进展。
结论
尿刊酸异构化不太可能是紫外线B介导的对实验性自身免疫性脑脊髓炎的抑制作用的原因。需要开展更多工作来研究紫外线B抑制疾病的其他机制。
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