ABSTRACT
The term “vitamin A” is the generic term for a group of fat-soluble compounds with the biological activity of retinol and commonly refers to retinol, retinaldehyde, and retinoic acid (RA). The relationship between vitamin A and the lung has been known since the early 20th century. Soon after the discovery of vitamin A in 1913 by McCollum and Davis who observed that the ether extract of egg or butter had a fat-soluble organic substance essential to nutrition in rats (1), McCollum (2) observed in 1917 that animals deficient in “fat-soluble factor A” quite “frequently suffered from prevalent bronchitis.” Bloch (3) observed that infants suffering from xerophthalmia frequently had respiratory infections and a higher risk of death and that the provision of milk, cream, and butter could reduce eye disease, promote growth and development, and reduce infectious disease in children. Mori (4) observed histological changes in the larynx and trachea and a high incidence of bronchopulmonary inflammatory lesions in retinol-deficient rats. In 1925, Wolbach and Howe observed squamous metaplasia of the normal mucus-secreting epithelium and occlusion of bronchi with desquamated cells in retinol-deficient rats (5). Research over the past few decades has defined some of the underlying mechanisms for these observations and clarified the critical role of vitamin A in lung development, maturation, inflammation, and repair from injury.
