Abstract
We first examined whether vitamin A improved the mucosal immune depression in mice with wasting protein deficiency. Mice fed a low-protein diet had lower concentrations of IgA, IL-4 and IL-5 in the small-intestinal mucosa than mice fed a 20% protein diet. Daily supplementation of 1mg of retinyl acetate significantly restored the IgA level in protein-deficient mice in parallel with an increase of the IL-5 level in the mucosa. In protein-deficient mice immunized with cholera toxin (CT), retinyl acetate also prevented the decline of the CT-specific IgA level, improving their survival rate after exposure to a high dose of CT. These results suggest that large oral supplements of vitamin A may preserve the mucosal IgA level during protein malnutrition, possibly by stimulating IL-5 production. To test this hypothesis, we next studied the effects of vitamin A on the mucosal IgA level in mice with artificially blocking of the IL-5 signaling pathway. Supplements of retinyl acetate did not increase the IgA level in the small-intestinal mucosa of IL-5 receptor α-chain-deficient (IL-5Rα-/-) mice, whereas it increased the IL-5 level in their small-intestinal mucosa. Retinyl acetate also failed to improve the survival rate of IL-5Rα-/- mice after exposure to a high dose of CT. Our data suggest that the effect of vitamin A on the mucosal IgA system may require the cooperation of IL-5.
