Vitamin D and Innate Immunity

White, John H.

doi:10.1016/b978-0-12-381978-9.10091-5

Cited by 4 publications

(3 citation statements)

References 121 publications

(119 reference statements)

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“…Among the many functions of 1,25-dihydroxyvitamin D 3 is the modulation of innate and adaptive immune responses. Calcitriol binds to VDR and recognizes cognate DNA motifs called vitamin D response elements in the nucleus of the cell, with high affinity inducing different responses (White, 2011). For instance, in activated human B cells, 25-hydroxyvitamin D 3 and 1,25-dihydroxyvitamin D 3 increased IL-10 production 3-fold (Heine et al, 2008), and IL-10 can promote B-cell differentiation into plasmablasts to secrete immunoglobulin (Defrance et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Effects of prepartum dietary cation-anion difference and source of vitamin D in dairy cows: Lactation performance and energy metabolism

Martínez

Rodney

Block³

et al. 2018

Journal of Dairy Science

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The objectives of this experiment were to evaluate the effects of feeding diets with 2 dietary cation-anion difference (DCAD) levels and supplemented with either cholecalciferol (CH) or calcidiol (CA) during late gestation on lactation performance and energetic metabolism in dairy cows. The hypothesis was that combining a prepartum acidogenic diet with calcidiol supplementation would benefit peripartum Ca metabolism and, thus, improve energy metabolism and lactation performance compared with cows fed an alkalogenic diet or cholecalciferol. Holstein cows at 252 d of gestation were blocked by parity (28 nulliparous and 51 parous cows) and milk yield within parous cows, and randomly assigned to 1 of 4 treatments arranged as a 2 × 2 factorial, with 2 levels of DCAD (positive, +130, and negative, -130 mEq/kg) and 2 sources of vitamin D, CH or CA, fed at 3 mg per 11 kg of diet dry matter (DM). The resulting treatment combinations were positive DCAD with CH (PCH), positive DCAD with CA (PCA), negative DCAD with CH (NCH), or negative DCAD with CA (NCA), which were fed for the last 21 d of gestation. After calving, cows were fed the same lactation diet. Body weight and body condition were evaluated prepartum and for the first 49 d postpartum. Blood was sampled thrice weekly prepartum, and on d 0, 1, 2, 3, and every 3 d thereafter until 30 d postpartum for quantification of hormones and metabolites. Lactation performance was evaluated for the first 49 d postpartum. Feeding a diet with negative DCAD reduced DM intake in parous cows by 2.1 kg/d, but no effect was observed in nulliparous cows. The negative DCAD reduced concentrations of glucose (positive = 4.05 vs. negative = 3.95 mM), insulin (positive = 0.57 vs. negative = 0.45 ng/mL), and insulin-like growth factor-1 (positive = 110 vs. negative = 95 ng/mL) prepartum. Treatments did not affect DM intake postpartum, but CA-supplemented cows tended to produce more colostrum (PCH = 5.86, PCA = 7.68 NCH = 6.21, NCA = 7.96 ± 1.06 kg) and produced more fat-corrected milk (PCH = 37.0, PCA = 40.1 NCH = 37.5, NCA = 41.9 ± 1.8 kg) and milk components compared with CH-supplemented cows. Feeding the negative DCAD numerically increased yield of fat-corrected milk by 1.0 kg/d in both nulliparous and 1.4 kg/d in parous cows. Minor differences were observed in postpartum concentrations of hormones and metabolites linked to energy metabolism among treatments. Results from this experiment indicate that replacing CH with CA supplemented at 3 mg/d during the prepartum period improved postpartum lactation performance in dairy cows.

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Section: Discussionmentioning

confidence: 99%

Effects of prepartum dietary cation-anion difference and source of vitamin D in dairy cows: Lactation performance and energy metabolism

Martínez

Rodney

Block³

et al. 2018

Journal of Dairy Science

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“…Its deficiency impairs innate immune response to Mycobacterium tuberculosis via toll-like receptor (TLR)-2 and nucleotide oligomerization domain (NOD)-2 which recognize triacylated lipoprotein and muramyl dipeptide from M. tuberculosis , respectively in monocytes and macrophages. Vitamin D increases expression of NOD-2 and its induction of human defensin beta 2, production of cathelicidin antimicrobial peptides (hCAP18, LL37) and autophagy in macrophages infected with mycobacteria 75 . Vitamin D also enhances generation of reactive oxygen and nitrogen species in leukocytes 76 , as well as enhances epithelial barrier function and chemokine secretion, 76, 77 .…”

Section: Vitamin Dmentioning

confidence: 99%

Vitamin E and D regulation of allergic asthma immunopathogenesis

Cook‐Mills

Avila

2014

International Immunopharmacology

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Asthma occurs as complex interactions of the environmental and genetics. Clinical studies and animal models of asthma indicate dietary factors such as vitamin E and vitamin D as protective for asthma risk. In this review, we discuss opposing regulatory functions of tocopherol isoforms of vitamin E and regulatory functions of vitamin D in asthma and how the variation in global prevalence of asthma may be explained, at least in part, by these dietary components.

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“…Vitamin D deficiency may have additional indirect effects on skeletal development due to its complex role in supporting immune responses (e.g., Hewison, ; Liu, ). Numerous immune cells are capable of initiating the additional synthesis of vitamin D which in turn, activates receptor signaling to enhance immune responses (Bikle, ; Kamen & Tangpricha, ; White, ). A period of deficiency can affect child health by limiting immune reactions and this has been particularly demonstrated with respiratory and gastrointestinal infections (Ginde, Mansbach, & Camargo, ; Ives, in press; WHO, ).…”

Section: Introductionmentioning

confidence: 99%

Endochondral growth disruption during vitamin D deficiency rickets in a mid‐19th century series from Bethnal Green, London, UK

Ives

Humphrey

2018

American J Phys Anthropol

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Pronounced growth faltering existed in children with active rickets and affected the upper and lower limb, indicating systemic growth failures during the deficiency. Poor maternal health, early weaning and inadequate infant feeding, and lack of sunlight exposure likely contributed to the development of rickets. Complex interactions between pathological conditions, nutritional deficiencies and vitamin D deficiency may have exacerbated growth impacts.

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Vitamin D and Innate Immunity

Cited by 4 publications

References 121 publications

Effects of prepartum dietary cation-anion difference and source of vitamin D in dairy cows: Lactation performance and energy metabolism

Effects of prepartum dietary cation-anion difference and source of vitamin D in dairy cows: Lactation performance and energy metabolism

Vitamin E and D regulation of allergic asthma immunopathogenesis

Endochondral growth disruption during vitamin D deficiency rickets in a mid‐19th century series from Bethnal Green, London, UK

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