Influence of 1,25-dihydroxy vitamin D3 on TLR4-induced activation of antigen presenting cells is dependent on the order of receptor engagement

Gambhir, Vandana; Kim, Julia; Siddiqui, Sarah; Taylor, Michelle; Byford, Valarie; Petrof, Elaine O.; Jones, Glenville; Basta, Sameh

doi:10.1016/j.imbio.2011.03.011

Cited by 30 publications

(21 citation statements)

References 45 publications

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“…These findings are in accordance with a study indicating that vitamin D deficiency is greatly associated with the early stages of OA but absent in the advanced stages [4]. This could be explained by a recent report indicating that vitamin D precedes the TLR activation, with no effect observed when vitamin D is administrated at the same time or after TLR stimulation [32]. These data and our data suggest that vitamin D supplementation must be administrated before cartilage damage occurs.…”

Section: Discussionsupporting

confidence: 93%

Effects of Vitamin D Supplementation during the Induction and Progression of Osteoarthritis in a Rat Model

Castillo

Hernandez-Cueto

Vega-Lopez

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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Epidemiological studies correlate low levels of vitamin D with the osteoarthritis (OA) progression. Cytokines and metalloproteases play a major role in OA promoting the inflammation and degradation of the cartilage and can be induced through the Toll-like receptor (TLR) pathway. The aim of this study was to evaluate the protective effect of vitamin D supplementation on the development of osteoarthritis (OA) through examining the genetic regulation of TLRs, cytokines, and metalloproteases in chondrocytes as well as the wideness of cartilage in rats with OA. Our results demonstrate that the signaling through TLR-4 is a proinflammatory mechanism in osteoarthritis that drives the upregulation of MMP-3, IL-1β, and TNF-α gene expression, leading to cartilage degradation and inflammation. Vitamin D supplementation had a protective effect during the onset but not during the chronic stage of OA in the rat model.

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Section: Discussionsupporting

confidence: 93%

Effects of Vitamin D Supplementation during the Induction and Progression of Osteoarthritis in a Rat Model

Castillo

Hernandez-Cueto

Vega-Lopez

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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“…Vitamin D has been demonstrated to down regulate TLR4 in liver cells, human monocytes THP-1, antigen-presenting cells and keratinocytes, resulting in a lower inflammatory response and reduced apoptosis (13–15,29). While hyperoxia upregulated the expression of TLR4, vitamin D treatment significantly attenuated this increase, and thereby exerted its anti-inflammatory and anti-apoptotic functions.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin D-knockout mice experience a more severe inflammatory response than wild-type mice after LPS treatment (12). The regulatory effect of vitamin D and its receptor on TLR4 has been demonstrated in many studies (13–15). Our previous study also found that vitamin D could significantly relieve LPS-induced lung injury (11).…”

Section: Introductionmentioning

confidence: 97%

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Yao

Shi

Zhao

et al. 2017

International Journal of Molecular Medicine

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With considerable morbidity and mortality, bron-chopulmonary dysplasia (BPD) is a focus of attention in neonatology. Hyperoxia-induced lung injury has long been used as a model of BPD. Among all the signaling pathways involved, Toll-like receptor 4 (TLR4) has been demonstrated to play an important role, and is known to be regulated by vitamin D. This study aimed at elucidating the effect of vitamin D on hyperoxia-induced lung injury and the role of TLR4 in the process. Vitamin D was administered to hyperoxia-treated neonatal rats to investigate changes in the morphology of lungs and expression of pro-inflammatory cytokines, apoptotic proteins and TLR4. Vitamin D attenuated hyperoxia-induced lung injury by protecting the integrity of the lung structure, decreasing extracellular matrix deposition and inhibiting inflammation. The upregulation of TLR4 by hyperoxia was ameliorated by vitamin D and apoptosis was reduced. Vitamin D administration antagonized the activation of TLR4 and therefore alleviated inflammation, reduced apoptosis and preserved lung structure.

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“…Of note, 1,25(OH) 2 D 3 can only induce this tolerogenic phenotype in DCs when it is added before their maturation. Once a maturation stimulus like lipopolysaccharide (LPS) is present or when the cells have already matured, the effects of 1,25(OH) 2 D 3 on DCs are minimal (133). Aside from in vitro differentiated DCs, 1,25(OH) 2 D 3 also induces a tolerogenic phenotype in dermal DCs, Langerhans cells, and plasmacytoid DCs, even though there are subtle differences between the effects on these subsets (100, 134, 135).…”

Section: Immune Modulation By Vitamin Dmentioning

confidence: 99%

Vitamin D in Autoimmunity: Molecular Mechanisms and Therapeutic Potential

et al. 2017

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Over the last three decades, it has become clear that the role of vitamin D goes beyond the regulation of calcium homeostasis and bone health. An important extraskeletal effect of vitamin D is the modulation of the immune system. In the context of autoimmune diseases, this is illustrated by correlations of vitamin D status and genetic polymorphisms in the vitamin D receptor with the incidence and severity of the disease. These correlations warrant investigation into the potential use of vitamin D in the treatment of patients with autoimmune diseases. In recent years, several clinical trials have been performed to investigate the therapeutic value of vitamin D in multiple sclerosis, rheumatoid arthritis, Crohn’s disease, type I diabetes, and systemic lupus erythematosus. Additionally, a second angle of investigation has focused on unraveling the molecular pathways used by vitamin D in order to find new potential therapeutic targets. This review will not only provide an overview of the clinical trials that have been performed but also discuss the current knowledge about the molecular mechanisms underlying the immunomodulatory effects of vitamin D and how these advances can be used in the treatment of autoimmune diseases.

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Influence of 1,25-dihydroxy vitamin D3 on TLR4-induced activation of antigen presenting cells is dependent on the order of receptor engagement

Cited by 30 publications

References 45 publications

Effects of Vitamin D Supplementation during the Induction and Progression of Osteoarthritis in a Rat Model

Effects of Vitamin D Supplementation during the Induction and Progression of Osteoarthritis in a Rat Model

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Vitamin D in Autoimmunity: Molecular Mechanisms and Therapeutic Potential

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