Vitamin A prevents the decline in immunoglobulin A and Th2 cytokine levelsin small intestinal mucosa of protein-malnourished mice

Citation
T. Nikawa et al., Vitamin A prevents the decline in immunoglobulin A and Th2 cytokine levelsin small intestinal mucosa of protein-malnourished mice, J NUTR, 129(5), 1999, pp. 934-941
Citations number
36
Categorie Soggetti
Food Science/Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF NUTRITION
ISSN journal
00223166 → ACNP
Volume
129
Issue
5
Year of publication
1999
Pages
934 - 941
Database
ISI
SICI code
0022-3166(199905)129:5<934:VAPTDI>2.0.ZU;2-Q
Abstract
We examined whether vitamin A improved mucosal immune depression in mice wi th wasting protein deficiency. In male C3H/HeN mice fed a semi-purified 1% protein diet for 2 wk, plasma retinol and immunoglobulin A (IgA) concentrat ions in the small intestinal mucosa were 50 and 55%, respectively, of those in mice fed a semi-purified 20% protein diet, (P < 0.05). Daily supplement ation of 0.3 mg of retinyl acetate to protein-deficient mice for 2 wk incre ased the plasma retinol level to the value in the protein-sufficient mice. However, 1 mg/d of retinyl acetate was required to prevent the decline of t he IgA level caused by the protein deficiency. Mice fed the low-protein die t had lower concentrations of IL-4 and IL-5 in the small intestinal mucosa and fewer IL-4- and IL-5-containing cells in the lamina propria (P < 0.05). Retinyl acetate(1 mg) significantly restored the IL-5 level and the number of IL-4- and IL-5-containing cells. After immunization with 20 mu g of cho lera toxin (CT), the intestinal mucosa of protein-deficient mice contained significantly less CT-specific IgA than control mice. Treatment with 1 mg o f retinyl acetate prevented the decline of anti-CT IgA level in the protein -deficient mice, improving their survival rate after an exposure to 0.1 mg of CT. These results suggest that large oral supplements of vitamin A may p reserve mucosal IgA level during protein malnutrition, possibly by stimulat ing Th2 cytokine production and thereby, inducing resistance against infect ion.