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To assess the effects of marginal biotin deficiency on immune function and thereby evaluate immune function as a potential marker for impaired biotin status, we investigated immune function in a rat model during progression from sufficiency to moderate biotin deficiency. As immune function indicators, we assessed the IgG response to a vaccine and the cytokine responses and relative proportions of lymphocyte subpopulations in the immunocytes in blood, spleen and thymus. Neither phenotype nor organ redistribution of lymphocytes differed between biotin-deficient and biotin-sufficient rats. Assessment of immune function by mitogen T cell proliferation, mitogen-induced interferon-gamma and interleukin-4 levels, IgG antibody responses and natural killer cell activity were not significantly different in mild to moderately biotin-deficient rats compared with biotin-sufficient controls. The absence of effects on immune function was not attributable to failure to induce biotin deficiency; the rats exhibited unequivocal evidence of biotin deficiency, including reduced hepatic biotin and impaired leucine metabolism resulting from deficiency of the biotin-dependent enzyme methylcrotonyl-CoA carboxylase. We conclude that the immune markers examined are not promising candidates as indicators of mild to moderate deficiency in humans.

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 micromol 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 [(3)H]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, [(3)H]thymidine uptake by postsupplementation PBMC was 66 +/- 21% of the uptake by presupplementation PBMC (P < 0.05). Similarly, concentrations of interleukin-1beta (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-1beta and interleukin-2.

The prevalence of food allergy continues to rise, particularly in 'westernized' societies; it has been linked to the 'hygiene hypothesis' and the increased diversity of food consumption worldwide. The pathogenic mechanisms and Th1/Th2 paradigm are being closely examined with respect to the occurrence of inflammatory and injury/repair responses at different mucosal sites. Genetically modified plants as potential food sources and allergenicity are current topics of controversy.

A major peanut allergen, Ara h 2, is recognized by serum IgE from > 90% of patients with peanut hypersensitivity. Biochemical characterization of this allergen indicates that it is a glycoprotein of approximately 17.5 kDa. Using N-terminal amino acid sequence data from purified Ara h 2, oligonucleotide primers were synthesized and used to identify a clone (741 bp) from a peanut cDNA library. This clone was capable of encoding a 17.5-kDa protein with homology to the conglutin family of seed storage proteins. The major linear immunoglobulin E (IgE)-binding epitopes of this allergen were mapped using overlapping peptides synthesized on an activated cellulose membrane and pooled serum IgE from 15 peanut-sensitive patients. Ten IgE-binding epitopes were identified, distributed throughout the length of the Ara h 2 protein. Sixty-three percent of the amino acids represented in the epitopes were either polar uncharged or apolar residues. In an effort to determine which, if any, of the 10 epitopes were recognized by the majority of patients with peanut hypersensitivity, each set of 10 peptides was probed individually with serum IgE from 10 different patients. All of the patient sera tested recognized multiple epitopes. Three epitopes (aa27-36, aa57-66, and aa65-74) were recognized by all patients tested. In addition, these three peptides bound more IgE than all the other epitopes combined, indicating that they are the immunodominant epitopes of the Ara h 2 protein. Mutational analysis of the Ara h 2 epitopes indicate that single amino acid changes result in loss of IgE binding. Two epitopes in region aa57-74 contained the amino acid sequence DPYSP that appears to be necessary for IgE binding. These results may allow for the design of improved diagnostic and therapeutic approaches to peanut hypersensitivity.

Studies of the effects of yogurt on immunity and atopic diseases have suggested improvements in cytokine (interleukin-2 and interferon-gamma) responses and clinical scores in patients with allergic rhinitis. This study compares prospectively immune parameters of participants who received 16 oz of yogurt versus 16 oz of milk/day in a randomized cross-over design. Yogurt that contained live, active Lactobacillus bulgaricus and Streptococcus thermophilus or 2% milk was consumed for one month each. Twenty otherwise healthy adults with atopic histories documented by skin testing were enrolled. Immune studies were performed at the beginning and end of the two 1-month study phases, separated by a 2-week washout period. These studies included measurements of cellular, humoral, and phagocytic function. No adverse events were noted in either group. No significant improvements in any immune parameter were noted. The consumption of yogurt that contained the live active bacteria L bulgaricus and S thermophilus does not appear to enhance immune function in atopic individuals at the dosage and duration used in this study.