Vitamin-A deficiency severely compromises the integrity of mucosal epithelial cells in the respiratory, gastrointestinal, and uterine tracts. In the respiratory tract, ciliated columnar epithelium with mucus and goblet cells traps and removes inhaled microorganisms. In animals deficient in vitamin A, ciliated epithelial cells are replaced by stratified, keratinized epithelium, and there is a decrease in mucin. Similarly, in the small intestine, vitamin-A deficiency results in a loss of microvilli, goblet cells, and mucin. Other effects of vitamin-A deficiency on innate immunity include changes in epidermal keratins that disrupt skin barrier function; defects in chemotaxis, adhesion, phagocytosis, and the ability to produce reactive oxygen species in neutrophils; decreased number of NK cells and cytotoxicity; and a decrease in the expression of the receptor that recognizes Gram-negative bacteria as well as the secretion of inflammatory cytokines by macrophages and monocytes.
An adequate level of vitamin A is also necessary to support acquired immunity. The growth and activation of B cells require retinol. Pigs deficient in vitamin A synthesize less than one-tenth of the amount of antibody produced by pigs fed vitamin A fortified diets. Infection with Trichinella spiralisa normally induces a strong T helper type 2-like response (i.e., high levels of parasite-specific IgG and production of IL-4, IL-5, and IL-10), but in vitamin-A deficiency an inappropriately strong T helper type 1 like response (i.e., production of interferon-g and IL-12) is induced.
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