Vitamin A, infection, and immune function

In populations where vitamin A availability from food is low, infectious di seases can precipitate vitamin A deficiency by decreasing intake, decreasin g absorption, and increasing excretion. Infectious diseases that induce the acute-phase response also impair the assessment of vitamin A status by tra nsiently depressing serum retinol concentrations. Vitamin A deficiency impa irs innate immunity by impeding normal regeneration of mucosal barriers dam aged by infection, and by diminishing the function of neutrophils, macropha ges, and natural killer cells. Vitamin A is also required for adaptive immu nity and plays a role in the development of both T-helper (Th) cells and B- cells. In particular, vitamin A deficiency diminishes antibody-mediated res ponses directed by Th2 cells, although some aspects of Th1-mediated immunit y are also diminished. These changes in mucosal epithelial regeneration and immune function presumably account for the increased mortality seen in vit amin A-deficient infants, young children, and pregnant women in many areas of the world today.