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ARS Home » Pacific West Area » Davis, California » Western Human Nutrition Research Center » Diet, Microbiome and Immunity Research » Research » Publications at this Location » Publication #257533
Title: Prenatal zinc supplementation of zinc-adequate rats adversely affects immunity in offspring

Author
item SHARKAR, M TOFAEL KABIR - International Centre For Diarrhoeal Disease Research
item JOU, MING-YU - University Of California
item HOSSAIN, MOHAMMAD - International Centre For Diarrhoeal Disease Research
item LONNERDAL, BO - University Of California
item Stephensen, Charles
item RAQUIB, RUBHANA - International Centre For Diarrhoeal Disease Research

Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/1/2011
Publication Date: 8/1/2011
Citation: Sharkar, M., Jou, M., Hossain, M.B., Lonnerdal, B., Stephensen, C.B., Raquib, R. 2011. Prenatal zinc supplementation of zinc-adequate rats adversely affects immunity in offspring. Journal of Nutrition. 141(8):1559-1564.

Interpretive Summary: Zinc deficiency increases the risk of developing infectious disease, including diarrheal disease, probably by impairing immune function. Thus zinc supplementation of infants, and perhaps pregnant women, is a potential way to decrease morbidity in infants. This paper reports the results of zinc supplementation on immune function of zinc-deficient and zinc-replete infant rats. The study showed that supplementation of pregnant rats with normal zinc status with additional zinc supplements during pregnancy had suppressive effects on cellular immune function in the intestinal tract for the offspring. These effects occurred when offspring were exposed to excess zinc during pregnancy and during lactation. This finding highlights the necessity of knowing the zinc status of subjects before zinc supplementation is recommended in order to prevent potential adverse effects.

Technical Abstract: We previously showed that zinc (Zn) supplementation of Zn-adequate dams induced immunosuppressive effects that persist in the offspring after weaning. We investigated whether the immunosuppressive effects were due to in utero exposure and/or mediated via milk using a cross-fostering design. Pregnant rats with adequate Zn nutriture were supplemented with either Zn (1.5 mg Zn in 10% sucrose) or placebo (10% sucrose) during pregnancy (3 times/wk). At postnatal d 3, 4 pups of Zn-supplemented dams (Zn-P) were exchanged with 4 of placebo-supplemented dams (P-Zn). The remaining pups continued with their biological mothers (Zn-Zn and P-P). Pups were orally immunized with dinitrophenol ovalbumin-BSA and/or cholera toxin B subunit (CTB), and serum Zn concentrations and cellular and humoral responses were assessed. Pups of Zn-supplemented dams had higher serum Zn when fostered either by placebo- or Zn-supplemented dams compared to pups of placebo-supplemented dams (P < 0.01). Postnatal Zn exposure reduced the number of Peyer's patches in both the Zn-Zn and P-Zn groups (P < 0.01). Prenatal Zn exposure suppressed CTB- (P = 0.05) and BSA-specific proliferation response of Peyer's Patch lymphocytes (P = 0.07). Prenatal Zn exposure effects on the splenocyte cytokine response were differently influenced by fostering mothers' Zn status. Antigen presenting cell (APC) activity of splenocytes was lower in the Zn-Zn group than in the P-P group (P < 0.08). In conclusion, prenatal Zn exposure increases serum Zn levels in pups and suppresses antigen-specific proliferation and antibody responses and APC function, whereas postnatal exposure may suppress the mucosal immune reservoir.