IMPAIRED MUCOSAL ANTIBODY-RESPONSE TO CHOLERA-TOXIN IN VITAMIN-A-DEFICIENT RATS IMMUNIZED WITH ORAL CHOLERA VACCINE

Citation
U. Wiedermann et al., IMPAIRED MUCOSAL ANTIBODY-RESPONSE TO CHOLERA-TOXIN IN VITAMIN-A-DEFICIENT RATS IMMUNIZED WITH ORAL CHOLERA VACCINE, Infection and immunity, 61(9), 1993, pp. 3952-3957
Citations number
33
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
61
Issue
9
Year of publication
1993
Pages
3952 - 3957
Database
ISI
SICI code
0019-9567(1993)61:9<3952:IMATCI>2.0.ZU;2-A
Abstract
To investigate the importance of vitamin A in the ability to respond t o oral antigen administration, rats were fed a vitamin A-free diet. Th e animals were immunized perorally three times with a mixture of chole ra toxin (CT) and a commercial cholera vaccine. The total immunoglobul in A (IgA) concentration as well as the specific IgA anti-CT antibody levels in serum and bile was significantly lower in the vitamin A-defi cient animals than in the paired fed controls (animals that were fed a normal commercial diet in an amount equal to the amount the deficient animals consumed), while the levels of total and specific anti-CT IgG were not affected to the same extent by the vitamin A deficiency. The number of IgA anti-CT antibody-producing cells in the mesenteric lymp h nodes after immunization was also significantly lower in the vitamin A-deficient rats than in the control rats. Supplementation of the die t with retinyl palmitate restored the ability to mount an IgA antibody response to the antigen, since the level of specific IgA anti-CT anti bodies in relation to the total IgA concentration was as high in the v itamin A-supplemented group as in the paired fed control group. Restri cted diet intake by itself did not affect the ability to respond adequ ately to the antigen since there was no difference in IgA anti-CT anti body level between paired fed rats and those being fed ad libitum. Ass essment of transforming growth factor beta in cell cultures revealed n o difference between vitamin A-deficient and paired fed animals. In su mmary, vitamin A deficiency resulted in a decreased number of IgA-prod ucing cells, decreased IgA production, and a reduced ability to respon d with IgA antibodies to the oral cholera vaccine.