Cord Blood 25-Hydroxyvitamin D3 and Allergic Disease During Infancy

Jones, Anderson P.; Palmer, Debra J.; Zhang, Guicheng; Prescott, Susan L.

doi:10.1542/peds.2012-1172

Cited by 135 publications

(170 citation statements)

References 29 publications

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“…A large number of observational studies subsequently linked vitamin D deficiency with a broad range of undesirable metabolic, immune and clinical outcomes (6,7). These include the risk of developing and/or surviving cancer (8)(9)(10), influenza epidemics (11), other respiratory infections (12)(13)(14), asthma (15)(16)(17)(18)(19), food allergies (20), inflammatory bowel diseases (21), obesity (22) and several chronic inflammatory disorders (6,23). One consequence of such research has been that a high level of self-medication with exogenous vitamin D now occurs in many countries, much as extensive high-level vitamin C supplementation became popular for its presumed benefits on the common cold and cancer survival between 1970 and the late 1980s.…”

mentioning

confidence: 99%

Vitamin D [1,25(OH)2D3] Differentially Regulates Human Innate Cytokine Responses to Bacterial versus Viral Pattern Recognition Receptor Stimuli

Fitch

Becker

HayGlass

2016

The Journal of Immunology

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Vitamin D plays multiple roles in regulation of protective and maladaptive immunity. Although epidemiologic studies link poor in vivo 25(OH)D status to increased viral respiratory infections, we poorly understand how vitamin D affects viral pattern recognition receptor (PRR)-driven cytokine production. In this study, we hypothesized that the biologically active metabolite of vitamin D, 1,25(OH)2D3, inhibits human proinflammatory and anti-inflammatory innate cytokine responses stimulated by representative bacterial or viral PRR ligands. Fresh PBMCs or CD14+ monocytes were stimulated with TLR4, TLR7/8-selective ligands, or respiratory syncytial virus (RSV) ± 1,25(OH)2D3. Proinflammatory and anti-inflammatory responses resulting from TLR4 stimulation were inhibited ∼50% in the presence of 1,25(OH)2D3. Conversely, its usage at physiologic through pharmacologic concentrations inhibited neither proinflammatory nor anti-inflammatory responses evoked by viral PRR ligands or infectious RSV. This differential responsiveness was attributed to the finding that TLR7/8, but not TLR4, stimulation markedly inhibited vitamin D receptor mRNA and protein expression, selectively reducing the sensitivity of viral PRR responses to modulation. 1,25(OH)2D3 also enhanced expression of IkBa, a potent negative regulator of NF-κB and cytokine production, in TLR4-stimulated monocytes while not doing so upon TLR7/8 stimulation. Thus, 1,25(OH)2D3 inhibits both proinflammatory and a broad panel of anti-inflammatory responses elicited by TLR4 stimulation, arguing that the common view of it as an anti-inflammatory immune response modifier is an oversimplification. In viral responses, it consistently fails to modify TLR7/8- or RSV-stimulated innate cytokine production, even at supraphysiologic concentrations. Collectively, the data call into question the rationale for increasingly widespread self-medication with vitamin D supplements.

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mentioning

confidence: 99%

Vitamin D [1,25(OH)2D3] Differentially Regulates Human Innate Cytokine Responses to Bacterial versus Viral Pattern Recognition Receptor Stimuli

Fitch

Becker

HayGlass

2016

The Journal of Immunology

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“…Low cord blood 25-OH-D3 was found as a risk factor for eczema at 1-year old [34]. Cord blood vitamin D level and multi-trigger wheezing, wheezing and risk of troublesome lung symptoms development have been reported to be reversely correlated in three different studies [35,36].…”

Section: Natal Umblical Cord Vitamin D Level and Wheezing Developmentmentioning

confidence: 95%

Vitamin D and Allergy

Özdemir¹

2016

MOJI

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After the modern vitamin D hypothesis firstly suggested in 1999 for the allergy pandemic, numerous conditions have been thought to be associated with vitamin D deficiency such as allergy, autoimmunity and neoplasm. Consistently, previous observational studies have linked lower vitamin D status to increased markers of atopy and allergic diseases e.g. atopic dermatitis, anaphylaxis and food allergy. Vitamin D is a "hormone" having important immunomodulatory and immunoregulatory properties. In vitamin D deficient conditions, disrupted mucosal and skin complex integrity and intercurrent infections may act synergistically with allergenic exposure to amplify sensitization risk. There has been emerging data to show that vitamin D can enhance the anti-inflammatory effects of glucocorticoids and potentially be used as adjuvant therapy in steroid-resistant severe asthma. And recent in vivo data suggest that vitamin D supplementation reduce the severity of eczema and allergic rhinitis as well as urticaria symptoms. However, there is presently inadequate evidence to support daily vitamin D supplementation in the prevention and/or treatment of allergic diseases in infants, children and adolescents.

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“…It has been shown that serum levels of vitamin D correlate with pulmonary function, asthma onset, and the development of allergic diseases. Based on clinical and observational data, the plasma level of 25(OH)D may serve as a "marker" to detect or define a subclinical deficiency of vitamin D [30]. It has recently been demonstrated that lower levels of vitamin D are associated with reduced asthma control.…”

Section: Association Of Allergic Sensitization and Vitamin Dmentioning

confidence: 99%

Immunomodulatory Effect of Vitamin D in Children with Allergic Diseases

Stelmach¹,

Jerzyńska²,

Podlecka³

2017

A Critical Evaluation of Vitamin D - Basic Overview

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The discovery that many cells express vitamin D receptors and the recognition of widespread vitamin D insufficiency has stimulated interest in the potential role of vitamin D in nonskeleton conditions. There is an increasing evidence to support the role of vitamin D pathway in the regulation of the function of both innate and adoptive immune systems. Vitamin D regulates immune function by inhibiting the differentiation and maturation of human dendritic cells, enhancing interleukin (IL)-10 and tumor growth factor-β (TGF-β) secretion and inhibiting T-cell functions. Vitamin D has the ability to suppress inflammatory cytokines, such as tumor necrosis factor (TNF), interleukin-1 (IL-1), interferon gamma (IFN-γ), and interleukin-2 (IL-2), while it increases the generation of anti-inflammatory cytokines IL-4 and IL-10. In B cells, vitamin D3 has also been shown to suppress immunoglobulin E (IgE) antibody class switch partly through the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB).

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Cord Blood 25-Hydroxyvitamin D3 and Allergic Disease During Infancy

Abstract: Reduced vitamin D status in pregnancy may be a risk factor for the development of eczema in the first year of life, reinforcing the need to explore the role of vitamin D exposure during development for disease prevention.

Cited by 135 publications

References 29 publications

Vitamin D [1,25(OH)2D3] Differentially Regulates Human Innate Cytokine Responses to Bacterial versus Viral Pattern Recognition Receptor Stimuli

Vitamin D [1,25(OH)2D3] Differentially Regulates Human Innate Cytokine Responses to Bacterial versus Viral Pattern Recognition Receptor Stimuli

Vitamin D and Allergy

Immunomodulatory Effect of Vitamin D in Children with Allergic Diseases

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