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Department of Nutritional Science and Dietetics, University of Nebraska at Lincoln, Lincoln, NE 68583;
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Department of Pediatrics, Division of Allergy and Immunology, Arkansas Childrens Hospital Research Institute, Little Rock, AR 72202; and
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, AR 72205
2To whom correspondence should be addressed. E-mail: mockdonaldm{at}exchange.uams.edu.
Theoretically, vitamin supplements may either enhance or reduce protein synthesis and proliferation in peripheral blood mononuclear cells (PBMC). In the present study, we determined whether administration of a pharmacologic dose of biotin affects proliferation rates of PBMC and cytokine release. Healthy adults (n = 5) ingested 3.1 µmol biotin/d for 14 d; blood and urine were collected pre- and postsupplementation. PBMC were isolated by density gradient and incubated with the mitogen concanavalin A for up to 3 d. At timed intervals during mitogen stimulation, we measured the following: 1) cellular uptake of [3H]thymidine to determine proliferation rates; 2) concentrations of various cytokines released into the medium; and 3) the percentages of PBMC subsets as judged by CD surface markers. Biotin supplementation caused a significant decrease of PBMC proliferation. At 2 d after mitogen stimulation, [3H]thymidine uptake by postsupplementation PBMC was 66 ± 21% of the uptake by presupplementation PBMC (P < 0.05). Similarly, concentrations of interleukin-1ß (2 d after mitogen) and interleukin-2 (1 d after mitogen) in media from postsupplementation PBMC were 65 ± 28% and 44 ± 23%, respectively, of those for presupplementation PBMC (P < 0.01). Percentages of PBMC subsets were not affected by 14 d of biotin supplementation. Overall, this study provides evidence that administration of pharmacologic doses of biotin for 14 d decreases PBMC proliferation and synthesis of interleukin-1ß and interleukin-2.
KEY WORDS: biotin cytokines humans lymphocytes proliferation
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