A Case of Anaphylaxis to Intramuscular but Not to Oral Application of Thiamine (Vitamin B1).

We report a 78 year-old non-atopic female with polyneuropathy who started to receive monthly intramuscular injections of thiamine hydrochloride. She had an anaphylaxis after the fourth injection. Skin prick test (SPT) with pure commercially available aqueous preparations was positive for thiamine hydrochloride. A titrated, single blinded, placebo-controlled oral provocation test with thiamine hydrochloride was well tolerated. The patient was then diagnosed as compartment allergy with hypersensitivity to parenteral but not to oral thiamine. Because in our patient, oral intake of thiamine has never been reported to lead to any adverse reaction. Oral tolerability might be due to the uptake mechanism of thiamine in the gastrointestinal system.

Metabolic changes during B cell differentiation for the production of intestinal IgA antibody.

To sustain the bio-energetic demands of growth, proliferation, and effector functions, the metabolism of immune cells changes dramatically in response to immunologic stimuli. In this review, I focus on B cell metabolism, especially regarding the production of intestinal IgA antibody. Accumulating evidence has implicated not only host-derived factors (e.g., cytokines) but also gut environmental factors, including the possible involvement of commensal bacteria and diet, in the control of B cell metabolism during intestinal IgA antibody production. These findings yield new insights into the regulation of immunosurveillance and homeostasis in the gut.

Mode of Bioenergetic Metabolism during B Cell Differentiation in the Intestine Determines the Distinct Requirement for Vitamin B1.

Bioenergetic metabolism varies during cell differentiation, but details of B cell metabolism remain unclear. Here, we show the metabolic changes during B cell differentiation in the intestine, where B cells differentiate into IgA(+) plasma cells (PCs). Naive B cells in the Peyer's patches (PPs) and IgA(+) PCs in the intestinal lamina propria (iLP) both used the tricarboxylic acid (TCA) cycle, but only IgA(+) PCs underwent glycolysis. These metabolic differences reflected their dependencies on vitamin B1, an essential cofactor for the TCA cycle. Indeed, the diminished activity of the TCA cycle after dietary vitamin B1 depletion decreased the number of naive B cells in PPs without affecting IgA(+) PCs in the iLP. The maintenance of naive B cells by dietary vitamin B1 was required to induce-but not maintain-intestinal IgA responses against oral antigens. These findings reveal the diet-mediated maintenance of B cell immunometabolism in organized and diffuse intestinal tissues.

Frontiers in vitamin research: new antibodies, new data.

Since 2004, the anatomical distribution of vitamins in the monkey brain, studied using immunohistochemical techniques and new tools (specific antisera that discriminate different vitamins reasonably well), has been an ongoing research field. The visualization of immunoreactive structures containing vitamins (folic acid, riboflavin, thiamine, pyridoxal, and vitamin C) has recently been reported in the monkey brain (Macaca fascicularis), all these vitamins showing a restricted or very restricted distribution. Folic acid, thiamine, and riboflavin have only been observed in immunoreactive fibers, vitamin C has only been found in cell bodies (located in the primary somatosensory cortex), and pyridoxal has been found in both fibers and cell bodies. Perikarya containing pyridoxal have been observed in the paraventricular hypothalamic nucleus, the periventricular hypothalamic region, and in the supraoptic nucleus. The fibers containing vitamins are thick, smooth (without varicosities), and are of medium length or long, whereas immunoreactive cell bodies containing vitamins are round or triangular. At present, there are insufficient data to elucidate the roles played by vitamins in the brain, but the anatomical distribution of these compounds in the monkey brain provides a general idea (although imprecise and requiring much more study) about the possible functional implications of these molecules. In this sense, here the possible functional roles played by vitamins are discussed.

Vitamin B1 functions as an activator of plant disease resistance.

Vitamin B(1) (thiamine) is an essential nutrient for humans. Vitamin B(1) deficiency causes beriberi, which disturbs the central nervous and circulatory systems. In countries in which rice (Oryza sativa) is a major food, thiamine deficiency is prevalent because polishing of rice removes most of the thiamine in the grain. We demonstrate here that thiamine, in addition to its nutritional value, induces systemic acquired resistance (SAR) in plants. Thiamine-treated rice, Arabidopsis (Arabidopsis thaliana), and vegetable crop plants showed resistance to fungal, bacterial, and viral infections. Thiamine treatment induces the transient expression of pathogenesis-related (PR) genes in rice and other plants. In addition, thiamine treatment potentiates stronger and more rapid PR gene expression and the up-regulation of protein kinase C activity. The effects of thiamine on disease resistance and defense-related gene expression mobilize systemically throughout the plant and last for more than 15 d after treatment. Treatment of Arabidopsis ecotype Columbia-0 plants with thiamine resulted in the activation of PR-1 but not PDF1.2. Furthermore, thiamine prevented bacterial infection in Arabidopsis mutants insensitive to jasmonic acid or ethylene but not in mutants impaired in the SAR transduction pathway. These results clearly demonstrate that thiamine induces SAR in plants through the salicylic acid and Ca(2+)-related signaling pathways. The findings provide a novel paradigm for developing alternative strategies for the control of plant diseases.

[Effect of thiamine on the formation of immune response in toxic lesions of the liver]. / O vliianii tiamina na formirovanie immunnogo otveta pri toksicheskom porazhenii pecheni.

The authors studied the influence of various doses of thiamine on the formation of immune response in the animals with toxic affection of the liver. As revealed, thiamine in a dose of 400 microgram per kg of body weight inhibited the formation of the immune response in healthy rats, but failed to influence this process in the animals with toxic affection of the liver. Thiamine in a dose of 100 microgram per 100 g of body weight stimulated the formation of the immune response in healthy rats and in those poisoned with carbon tetrachloride. The simulating effect of thiamine was more pronounced in poisoned than in healthy rats. The blood serum of rats poisoned with carbon tetrachloride enhanced the immunostimulating action of thiamine.