Abstract
Nearly 80years ago at the University of Wisconsin, Mc Collum and Davis (1913) discovered a lipophilic, growth-supportings ubstance, and Steenbock et al. (1921) reported that rats ingesting a diet devoid of this substance, vitamin A, often died of respiratory infections. The increased morbidity and mortality due to infection was quickly confirmed in vitamin A deficient (VAD) rabbits, pigeons, and humans (Werkman 1923; Green and Mellanby 1928). Mortality from infection occurred before vitamin A deficiency signs (xerophthalmia, keratinization) appeared (Boynton and Bradford 1931; Mc Coy 1934). These early reports showing a causal relationship between vitamin A deficiency and predisposition to infection began to establish the cycle of malnutrition and infection (Fig. 1). Greene(1933) documented poor antigen-specific immunoglobulin (Ig) responses in VAD animals, and Bresse etal. (1942) discovered a causal relationship between infection and vitamin A depletion, completing the cycle. The challenge was then and is now to elucidate the molecular basis for the cycle of vitamin A deficiency, immune dysfunction, and infection, and to interrupt the cycle with nutritional intervention.
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Hayes, C.E., Nashold, F.E., Gomez, F.E., Hoag, K.A. (1999). Retinoids and Immunity. In: Nau, H., Blaner, W.S. (eds) Retinoids. Handbook of Experimental Pharmacology, vol 139. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58483-1_21
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