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  • Title: Effect of carotenoids on in vitro immunoglobulin production by human peripheral blood mononuclear cells: astaxanthin, a carotenoid without vitamin A activity, enhances in vitro immunoglobulin production in response to a T-dependent stimulant and antigen.
    Author: Jyonouchi H, Sun S, Gross M.
    Journal: Nutr Cancer; 1995; 23(2):171-83. PubMed ID: 7644386.
    Abstract:
    The effect of carotenoids on in vitro immunoglobulin (Ig) production by peripheral blood mononuclear cells (PBMNC) was examined by employing blood samples from adult volunteers and full-term newborn babies (umbilical cord blood). Under carotenoid-supplemented culture conditions, cells were stimulated by polyclonal stimulants, neoantigens, and a recall antigen (Ag), and IgM, IgA, and IgG levels in the culture supernatant were measured. Beta-carotene and astaxanthin were used as representatives of carotenoids with and without vitamin A activity, respectively. Astaxanthin enhanced IgM production in response to T-dependent Ag (TD-Ag) and a T-dependent polyclonal stimulant. Astaxanthin also augmented IgG production in response to a recall Ag. IgA production without supplemental carotenoids was negligible for all stimuli. However, in carotenoid-supplemented cultures, IgA production was significantly higher in response to a T-dependent polyclonal stimulant than in unsupplemented cultures. IgM and IgA production was augmented at 10(-8) mol/l astaxanthin, whereas astaxanthin enhanced IgG production in response to a recall Ag at 10(-10)-10(-9) mol/l. Similar enhancing actions of astaxanthin on IgM production were observed in cord blood mononuclear cells (CBMNC), although CBMNC produced less IgM than adult PBMNC. Beta-carotene did not have a significant effect on human Ig production. The carotenoid actions were not demonstrated under serum-free culture conditions; serum is essential for solubilization of carotenoids. In summary, this study has shown for the first time that astaxanthin, a carotenoid without vitamin A activity, enhances human Ig production in response to T-dependent stimuli.
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