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尿刊酸和阳光在与蛋白质营养不良相关的免疫抑制中的潜在作用。

The potential role for urocanic acid and sunlight in the immune suppression associated with protein malnutrition.

作者信息

Hug D H, Hunter J K, Dunkerson D D

机构信息

Bacteriology Research Laboratory, Department of Veterans Affairs Medical Center, Iowa City, IA 52246, USA.

出版信息

J Photochem Photobiol B. 1998 Jul 10;44(2):117-23. doi: 10.1016/S1011-1344(98)00130-4.

Abstract

Irradiation of skin by sunlight or ultraviolet B (UVB, 290-320 nm) brings about a downregulation of cell-mediated immunity. An action spectrum for photoimmune suppression in mice indicates that trans-urocanic acid absorbs UV photons and is isomerized to the cis-isomer in the stratum corneum. Cis-urocanic acid is subsequently shown to suppress cellular immunity in mice. When histidine is elevated in a mouse diet, a higher level of urocanic acid is detected in mouse skin. These mice are more susceptible to photoimmune suppression. There is evidence that humans and animals experiencing protein malnutrition have very high levels of urocanic acid and/or histidine. Urocanic acid is formed by deamination of histidine in one enzymatic step. We discuss the protein malnutrition of kwashiorkor patients. They experience suppressed immunity and disturbed histidine metabolism. Here, we present a testable hypothesis: one cause of the immune deficiency observed in humans with protein malnutrition is the photoconversion by UVB of increased levels of trans-urocanic acid in skin to cis-urocanic acid, which suppresses the cellular immune system.

摘要

阳光或紫外线B(UVB,290 - 320纳米)对皮肤的照射会导致细胞介导免疫的下调。小鼠光免疫抑制的作用光谱表明,反式尿刊酸吸收紫外线光子并在角质层中异构化为顺式异构体。随后发现顺式尿刊酸可抑制小鼠的细胞免疫。当小鼠饮食中组氨酸含量升高时,在小鼠皮肤中检测到更高水平的尿刊酸。这些小鼠对光免疫抑制更敏感。有证据表明,经历蛋白质营养不良的人和动物体内尿刊酸和/或组氨酸水平非常高。尿刊酸是由组氨酸通过一步酶促脱氨作用形成的。我们讨论了夸休可尔症患者的蛋白质营养不良情况。他们免疫力受到抑制,组氨酸代谢紊乱。在此,我们提出一个可验证的假设:蛋白质营养不良的人类中观察到的免疫缺陷的一个原因是皮肤中升高的反式尿刊酸被UVB光转化为顺式尿刊酸,从而抑制细胞免疫系统。

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