Vitamin D and corticosteroids in asthma: synergy, interaction and potential therapeutic effects

Litonjua, Augusto A.

doi:10.1586/ers.12.85

Cited by 22 publications

(13 citation statements)

References 26 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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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 enhances steroid‐induced interleukin‐10 secretion and MAPK phosphatase 1 expression to produce increased anti‐inflammatory effects. Vitamin D also suppresses inflammation by enhancing both corticosteroid inhibition of proinflammatory chemokines such as RANTES (regulated upon activation normal T‐cell expressed and secreted) and corticosteroid induction of a tolerogenic dendritic cell phenotype 16 . But the current study by Zator et al is the first to specifically show the link between vitamin D status and anti‐TNFα therapy.…”

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confidence: 69%

Using Plasma Vitamin D Concentration as a Surrogate Marker to Predict Drug Response

Chan

Paski

2014

J Parenter Enteral Nutr

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“…Lastly, Litonjua,112 in his review, examined whether the administration of vitamin D enhances corticosteroid actions and potentially reverses steroid resistance, a crucial topic for asthmatic patients. As it has already been mentioned in the present review, several clinical and observational studies have suggested a synergistic effect of vitamin D and corticosteroids in asthma outcomes 83,92,93,96.…”

Section: Resultsmentioning

confidence: 99%

Vitamin D in asthma and future perspectives

Huang

Porpodis²,

Domvri³

et al. 2013

DDDT

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Humans have the ability to synthesize vitamin D during the action of ultraviolet (UV) radiation upon the skin. Apart from the regulation of calcium and phosphate metabolism, another critical role for vitamin D in immunity and respiratory health has been revealed, since vitamin D receptors have also been found in other body cells. The term “vitamin D insufficiency” has been used to describe low levels of serum 25-hydroxyvitamin D that may be associated with a wide range of pulmonary diseases, including viral and bacterial respiratory infection, asthma, chronic obstructive pulmonary disease, and cancer. This review focuses on the controversial relationship between vitamin D and asthma. Also, it has been found that different gene polymorphisms of the vitamin D receptor have variable associations with asthma. Other studies investigated the vitamin D receptor signaling pathway in vitro or in experimental animal models and showed either a beneficial or a negative effect of vitamin D in asthma. Furthermore, a range of epidemiological studies has also suggested that vitamin D insufficiency is associated with low lung function. In the future, clinical trials in different asthmatic groups, such as infants, children of school age, and ethnic minorities are needed to establish the role of vitamin D supplementation to prevent and/or treat asthma.

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Vitamin D and corticosteroids in asthma: synergy, interaction and potential therapeutic effects

Cited by 22 publications

References 26 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

Using Plasma Vitamin D Concentration as a Surrogate Marker to Predict Drug Response

Vitamin D in asthma and future perspectives

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