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.

CROSSTALK BETWEEN VITAMIN B AND IMMUNITY.

Vitamin B1 (thiamin) is considered to be the oldest vitamin and in 1936 R.R. Williams and colleagues determined its chemical structure and were able to synthesize this vitamin. Vitamin B1 influences pro-apoptotic proteins, mitochondrial membrane potential, cytochrome C release, protein kinases, p38-MAPK, suppresses oxidative stress-induced NF-kappaB and has anti-inflammatory properties. Deficiency of vitamin B1 may cause beriberi, dysfunction of the nervous system, neuroinflammation, T cell infiltration, chemokine CCL2 activation, over expression of proinflammatory cytokines, such as IL-1, TNF, IL-6, and arachidonic acid products, and induces expression of CD40 by the microglia and CD40L by astrocytes which provoke the death of neurons. Here we report the relationship between vitamin B complex and immunity.

Interaction of nutrition and infection: effect of vitamin B12 deficiency on resistance to Trypanosoma lewisi.

A metabolic imbalance technique was employed to study vitamin B(12) deficiency in rats infected with Trypanosoma lewisi. Throughout the observational period, animals on the deficient diet had lowered serum vitamin B(12) levels compared with complete and pair-fed animals. The decline in the level of the vitamin, ten days after the initiation of the experiment, continued progressively until the termination of the study. Body weight gains and food consumption in rats on complete, vitamin B(12)-deficient, or pair-fed diets and inoculated with T lewisi showed significant increase over inoculated controls. The rates of body weight and food consumption in vitamin B(12)-deficient animals were significantly less than that of the adequately fed animals.The indices of lowered resistance to infection in the vitamin B(12)-deficient rats were manifoid. Deficient rats suffered earlier and higher parasitemia followed by persistent infection. The delay in the synthesis of the reproductive inhibiting antibody (ablastin) resulted in prolonged variability in the length of the trypomastigotes. Severe depression in the primary and secondary antibody responses (IgG and IgM) to in vivo immunization of sheep erythrocytes was also observed in the deficient animals. In comparison, the level of IgG antibody decreased approximately one fifth the control values.

Role of the B vitamins in the immune response.

Studies conducted in our laboratory relating to the development of immune processes in B vitamin deficiency states of experimental animals have been reviewed. 1. The significant participation of certain of these nutritional factors in the production of circulating antibodies to a variety of antigens and the manifestation of delayed hypersensitivity reactions, including the rejection of tissue transplants, have been described. 2. Investigations on the mode of action of pyridoxine and pantothenic acid have demonstrated a marked reduction in the production of antibody-forming cells following antigenic stimulation in both deficiency states. The metabolism of antigen appeared to be normal. However, these two vitamins seem to function at different loci in the development of the immune process. Whereas pyridoxine appears to be necessary for the production of "C1" units from serine which are required for the biosynthesis of nucleic acids, it seems likely that pantothenic acid is involved in the secretion of newly-synthesized proteins into the extracellular compartment.

Malnutrition and susceptibility to infection with Vibrio cholerae in vervet monkeys (Cercopithecus aethiops). 2. Response of vervet monkeys on protein, B-vitamin complex and calorie-deficient diets to infection.

Five groups of vervet monkeys (Cercopithecus aethiops) were fed regular monkey chow, low protein (LP), low B-vitamin complex (LBV), LP-LBV, or low protein- low calorie (LP-LC) diets, respectively. After eight weeks the animals were infected with cholera vibrios. IgG, IgA and IgM increased in the sera of all animals after the challenge but the avidity of the immunoglobulins was lower in vervets on LP diets. Diarrhea and excretion of vibrios lasted longer in animals consuming less protein.