Science. 1939 Apr 21;89(2312):368-70. doi: 10.1126/science.89.2312.368.
Riboflavin deficiency, even in a relatively early stage, greatly lowers the resistance of the rat to endemic typhus, thereby resulting in a fatal disease. Not only the serosal cells, but also the endothelial cells in several organs, notably the Kupfer cells of the liver, become greatly distended with rickettsiae under these conditions. Preliminary experiments strongly suggest that advanced vitamin A deficiency, even when making animals markedly cachetic, does not have a comparable effect. Riboflavin deficient animals remain alive for several weeks with an abnormal intracellular metabolism. This type of deficiency is worthy of further study as a possible method of approach in the investigation of other intracellular parasites and filtrable viruses. Speculation regarding the mechanism concerned also suggests the desirability of a study of the effects of this deficiency upon the production of immune bodies in general.
核黄素缺乏症,即使在早期阶段,也会大大降低大鼠对地方性斑疹伤寒的抵抗力,从而导致致命的疾病。在这些条件下,不仅浆膜细胞,而且几个器官的内皮细胞,特别是肝脏的库普弗细胞,都会因立克次体而变得极度膨胀。初步实验强烈表明,即使维生素 A 严重缺乏使动物明显消瘦,也不会产生类似的效果。核黄素缺乏的动物在异常的细胞内代谢中仍能存活数周。这种类型的缺乏症值得进一步研究,作为研究其他细胞内寄生虫和可过滤病毒的一种可能方法。对相关机制的推测也表明,有必要研究这种缺乏症对一般免疫体产生的影响。