We examined the effect of advanced vitamin A deficiency (serum retinol < or = 0.35 micromol/L, with weight gain significantly lower than in controls with free access to food) on the secretory immunoglobulin A (IgA) response to a mild, upper respiratory tract infection with influenza A virus in BALB/c mice. Mice fed a vitamin A-deficient or control diet were infected intranasally at 11 to 12 wk of age. The influenza-specific salivary IgA response was lower in the vitamin A-deficient mice (0.11 +/- 0.13% of total IgA 4 wk after infection) than in controls with free access to food (2.73 +/- 1.86%, P < 0.0001). In a separate experiment, the response of vitamin A-deficient mice (0.42 +/- 1.51%) was also lower than that of pair-fed controls (3.43 +/- 4.76%, P < 0.0001). In addition, fewer influenza A-specific IgA-secreting plasma cells were found in the salivary glands of vitamin A-deficient mice (geometric mean 3.0%) than in controls with free access to food or in pair-fed controls (geometric mean 8.7%, P < 0.0001). Although the pathogen-specific IgA response was decreased, vitamin A-deficient mice had a significantly higher concentration of total salivary IgA (31.9 +/- 15.9 mg/L) than did the pair-fed controls (14.3 +/- 8.4 mg/L, P < 0.0001). Northern blot analysis of salivary gland RNA revealed that these vitamin A-deficient mice also had greater levels of mRNA of the polymeric immunoglobulin receptor (pIgR), which transports IgA across mucosal surfaces (plgR: beta-actin mRNA ratio = 7.8 +/- 0.8), than did pair-fed control mice (3.7 +/- 0.4, P = 0.0001). These data demonstrate that vitamin A deficiency has contrasting effects on the secretory IgA response to influenza infection, with a principal effect being a decrease in the pathogen-specific response.
Vitamin A deficiency results in a loss of Secretory IgA production during an infection. Keep in mind this was a mouse study (has certain limitations, but can still be useful). Secretory IgA in humans is important to prevent infections and leaky gut.