TY - JOUR
T1 - Vitamin a status and the antibody response to bacterial antigens
AU - Ross, A. Catharine
N1 - Funding Information:
This research was supported by NIH grant DK-41479 and funds from the Howard Heinz Endowment. These experiments were made possible through the ideas and efforts of Christopher E. Taylor, A.M.G. Pasatiempo, M. Kinoshita, S. Sri Kantha, T.A. Bowman, E.M. Gardner, D. Arora and Z. Zhao to whom the author extends her sincere thanks.
PY - 1996/5/2
Y1 - 1996/5/2
N2 - The antibody response of vitamin A-deficient rats was determined after immunization with bacterial antigens that differ in structure and immunological type. Primary antibody responses, measured as antigen-specific plaque-forming cells (PFC) or plasma immu-noglobulin (Ig) concentration, were significantly reduced in vitamin A-deficient rats immunized with polysaccharide antigens (pneumococcal or meningococcal types) or with protein antigens (tetanus toxoid or sheep red blood cells). In marked contrast, the antibody response to bacterial lipopolysaccharides was normal, even in animals with physical signs of deficiency. Because the response to polysaccharide and protein antigens is regulated by T lymphocytes while that to li-popolysaccharides is T cell-independent, these data suggest that impairments in T cell function may be responsible for the poor antibody responses. However, the number of T lymphocytes was unaffected, or only modestly changed. Also, antibody production per se was not impaired, as judged from the concentration of total plasma IgG and the normal response to lipopolysaccharides. In all instances of low antibody production, supplementation of vitamin A-deficient rats with doses of retinyl ester comparable to those used in children restored the antibody response to control values. For tetanus toxoid, a recall antigen, even when the primary antibody response was poor, immunologic memory was formed and, after repletion with retinol, the secondary anti-tetanus response was normal. During vitamin A deficiency, elicitation of cytokines by lipopolysac-charide, or injection of tumor necrosis factor-alpha, resulted in a marked increase in anti-tetanus IgG production. These data indicate that low vitamin A status reduces the ability to respond to antigens dependent on T lymphocytes but, at the same time, memory formation is not impaired; and that repletion with vitamin A, or provision of a strong cytokine stimulus to vitamin A-deficient rats, is sufficient to produce a normal or elevated antibody response.
AB - The antibody response of vitamin A-deficient rats was determined after immunization with bacterial antigens that differ in structure and immunological type. Primary antibody responses, measured as antigen-specific plaque-forming cells (PFC) or plasma immu-noglobulin (Ig) concentration, were significantly reduced in vitamin A-deficient rats immunized with polysaccharide antigens (pneumococcal or meningococcal types) or with protein antigens (tetanus toxoid or sheep red blood cells). In marked contrast, the antibody response to bacterial lipopolysaccharides was normal, even in animals with physical signs of deficiency. Because the response to polysaccharide and protein antigens is regulated by T lymphocytes while that to li-popolysaccharides is T cell-independent, these data suggest that impairments in T cell function may be responsible for the poor antibody responses. However, the number of T lymphocytes was unaffected, or only modestly changed. Also, antibody production per se was not impaired, as judged from the concentration of total plasma IgG and the normal response to lipopolysaccharides. In all instances of low antibody production, supplementation of vitamin A-deficient rats with doses of retinyl ester comparable to those used in children restored the antibody response to control values. For tetanus toxoid, a recall antigen, even when the primary antibody response was poor, immunologic memory was formed and, after repletion with retinol, the secondary anti-tetanus response was normal. During vitamin A deficiency, elicitation of cytokines by lipopolysac-charide, or injection of tumor necrosis factor-alpha, resulted in a marked increase in anti-tetanus IgG production. These data indicate that low vitamin A status reduces the ability to respond to antigens dependent on T lymphocytes but, at the same time, memory formation is not impaired; and that repletion with vitamin A, or provision of a strong cytokine stimulus to vitamin A-deficient rats, is sufficient to produce a normal or elevated antibody response.
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U2 - 10.1300/J053v04n01_04
DO - 10.1300/J053v04n01_04
M3 - Article
AN - SCOPUS:0029933760
SN - 1049-5150
VL - 4
SP - 47
EP - 75
JO - Journal of Nutritional Immunology
JF - Journal of Nutritional Immunology
IS - 1-2
ER -