ovalbumin and Vitamin-D-Deficiency

Topics: Allergens; Animals; Diarrhea; Disease Models, Animal; Female; Food Hypersensitivity; Immunoglobulin E; Immunoglobulin G; Interleukin-4; Lymph Nodes; Mice, Inbred BALB C; Ovalbumin; Vitamin D Deficiency

This study assessed bioavailability and utilisation of vitamin D3 in two feeding trials using young, growing Sprague-Dawley male rats. Trial one fed animals standard AIN-93G diet (casein protein) containing no vitamin D3 and goat or cow skimmed milk supplemented with vitamin D3. Trial two fed animals modified dairy-free AIN-93G diet (egg albumin) containing no vitamin D3 and goat or cow skimmed or full-fat milk supplemented with vitamin D3. Control groups received AIN-93G diets with or without vitamin D, and water. At 8 weeks of age, blood samples were collected for vitamin and mineral analysis, and femurs and spines were collected for assessment of bone mineralisation and strength. In both trials, analyses showed differences in bioavailability of vitamin D3, with ratios of serum 25-hydroxyvitamin D3 to vitamin D3 intake more than 2-fold higher in groups drinking supplemented milk compared with groups fed supplemented solid food. Bone mineralisation was higher in groups drinking supplemented milk compared with groups fed supplemented solid food, for both trials (P<0·05). There was no difference in the parameters tested between skimmed milk and full-fat milk or between cow milk and goat milk. Comparison of the two trials suggested that dietary protein source promoted bone mineralisation in a growing rat model: modified AIN-93G with egg albumin produced lower bone mineralisation compared with standard AIN-93G with casein. Overall, this study showed that effects of vitamin D3 deficiency in solid diets were reversed by offering milk supplemented with vitamin D3, and suggests that using milk as a vehicle to deliver vitamin D is advantageous.

Topics: Animals; Biological Availability; Bone Density; Calcifediol; Calcification, Physiologic; Calcium; Cattle; Cholecalciferol; Diet; Dietary Proteins; Dietary Supplements; Fats; Goats; Male; Milk; Ovalbumin; Rats; Rats, Sprague-Dawley; Recoverin; Vitamin D Deficiency

The vitamin D receptor participates in the control of IgE class-switch recombination in B cells. The physiologic vitamin D receptor agonist, 1,25(OH)

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; B-Lymphocytes; Bone Marrow; Calcitriol; Female; Helminthiasis, Animal; Immunoglobulin Class Switching; Immunoglobulin E; Immunoglobulin G; Intestinal Diseases, Parasitic; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Mice, Knockout; Nematospiroides dubius; Organ Specificity; Ovalbumin; Receptors, Calcitriol; Spleen; T-Lymphocytes; Vitamin D Deficiency

Vitamin D may be essential for restricting the development and severity of allergic diseases and asthma, but a direct causal link between vitamin D deficiency and asthma has yet to be established. We have developed a 'low dose' model of allergic airway disease induced by intraperitoneal injection with ovalbumin (1 µg) and aluminium hydroxide (0.2 mg) in which characteristics of atopic asthma are recapitulated, including airway hyperresponsiveness, antigen-specific immunoglobulin type-E and lung inflammation. We assessed the effects of vitamin D deficiency throughout life (from conception until adulthood) on the severity of ovalbumin-induced allergic airway disease in vitamin D-replete and -deficient BALB/c mice using this model. Vitamin D had protective effects such that deficiency significantly enhanced eosinophil and neutrophil numbers in the bronchoalveolar lavage fluid of male but not female mice. Vitamin D also suppressed the proliferation and T helper cell type-2 cytokine-secreting capacity of airway-draining lymph node cells from both male and female mice. Supplementation of initially vitamin D-deficient mice with vitamin D for four weeks returned serum 25-hydroxyvitamin D to levels observed in initially vitamin D-replete mice, and also suppressed eosinophil and neutrophil numbers in the bronchoalveolar lavage fluid of male mice. Using generic 16 S rRNA primers, increased bacterial levels were detected in the lungs of initially vitamin D-deficient male mice, which were also reduced by vitamin D supplementation. These results indicate that vitamin D controls granulocyte levels in the bronchoalveolar lavage fluid in an allergen-sensitive manner, and may contribute towards the severity of asthma in a gender-specific fashion through regulation of respiratory bacteria.

Topics: Aerosols; Allergens; Animals; Asthma; Bacteria; Bacterial Load; Bronchial Hyperreactivity; Bronchoalveolar Lavage Fluid; Dendritic Cells; Disease Models, Animal; Female; Granulocytes; Immunoglobulin E; Immunoglobulin G; Leukocyte Count; Lung; Lymph Nodes; Male; Mice; Mice, Inbred BALB C; Ovalbumin; RNA, Messenger; T-Lymphocytes; Vitamin D; Vitamin D Deficiency

There is debate as to whether vitamin D deficiency contributes towards the extent of the asthma epidemic. In this study, using a mouse model, we determined whether vitamin D deficiency in utero and during early life modulated the severity of asthma. Using dietary restriction, vitamin D(3) -replete and vitamin D(3) -deficient colonies of BALB/c mice were established. Utilizing the allergic airway disease model of asthma with the experimental allergen ovalbumin (OVA), we examined asthma-like responses 24 h after airway challenge with OVA in adult offspring born to vitamin D(3) -replete and vitamin D(3) -deficient mothers. The ability of airway-draining lymph node cells to proliferate and secrete cytokines in response to OVA ex vivo was significantly enhanced by vitamin D(3) deficiency. However, other aspects of allergic disease, including the numbers and proportions of inflammatory cells and cytokines in the lungs and the quantity of OVA-specific IgE in serum, were not modified. These results suggest that vitamin D(3) deficiency modulates the capacity of lymphocytes to respond to allergens.

Topics: Allergens; Animals; Asthma; Cholecalciferol; Cytokines; Female; Humans; Immunoglobulin E; Lung; Lymph Nodes; Lymphocytes; Mice; Mice, Inbred BALB C; Models, Animal; Ovalbumin; Vitamin D Deficiency