scholarly journals Vitamin D Signaling in the Context of Innate Immunity: Focus on Human Monocytes

2019 ◽  
Vol 10 ◽  
Author(s):  
Carsten Carlberg
Keyword(s):  
Vitamin D ◽  
Innate Immunity ◽  
Human Monocytes ◽  
Vitamin D Signaling

scholarly journals Vitamin D signaling maintains intestinal innate immunity and gut microbiota: potential intervention for metabolic syndrome and NAFLD

2020 ◽  
Vol 318 (3) ◽  
pp. G542-G553 ◽  
Author(s):  
Yilan Zeng ◽  
Mei Luo ◽  
Liwei Pan ◽  
Yuan Chen ◽  
Siqi Guo ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Vitamin D ◽  
Innate Immunity ◽  
Small Intestine ◽  
Bacterial Translocation ◽  
Paneth Cell ◽  
Distal Region ◽  
Dietary Vitamin ◽  
Experimental Investigations ◽  
Vitamin D Signaling

A lack of sunlight exposure, residence in the northern latitudes, and dietary vitamin D insufficiency are coprevalent with metabolic syndrome (MetS), Type 2 diabetes (T2D), and nonalcoholic fatty liver diseases (NAFLD), implying a potential causality and underlying mechanism. Whether vitamin D supplementation or treatment can improve these disorders is controversial, in part, because of the absence of large-scale trials. Experimental investigations, on the other hand, have uncovered novel biological functions of vitamin D in development, tumor suppression, and immune regulation, far beyond its original role as a vitamin that maintained calcium homeostasis. While the large intestine harbors massive numbers of microbes, the small intestine has a minimal quantity of bacteria, indicating the existence of a gating system located in the distal region of the small intestine that may restrain bacterial translocation to the small intestine. Vitamin D receptor (VDR) was found to be highly expressed at the distal region of small intestine, where the vitamin D signaling promotes innate immunity, including the expression of α-defensins by Paneth cells, and maintains the intestinal tight junctions. Thus, a new hypothesis is emerging, indicating that vitamin D deficiency may impair the intestinal innate immunity, including downregulation of Paneth cell defensins, leading to bacterial translocation, endotoxemia, systemic inflammation, insulin resistance, and hepatic steatosis. Here, we review the studies for vitamin D for innate immunity and metabolic homeostasis, and we outline the clinical trials of vitamin D for mitigating MetS, T2D, and NAFLD.

Impaired Vitamin D Signaling Is Associated With Frequent Development of Renal Cell Tumor in End-stage Kidney Disease

2020 ◽  
Vol 40 (11) ◽  
pp. 6525-6530
Author(s):  
JANOS DOCS ◽  
DANIEL BANYAI ◽  
TIBOR FLASKO ◽  
ARPAD SZANTO ◽  
GYULA KOVACS
Keyword(s):  
Vitamin D ◽  
Kidney Disease ◽  
Renal Cell ◽  
Cell Tumor ◽  
End Stage Kidney Disease ◽  
Vitamin D Signaling ◽  
End Stage

scholarly journals Vitamin D upregulates the macrophage complement receptor immunoglobulin in innate immunity to microbial pathogens

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Annabelle G. Small ◽  
Sarah Harvey ◽  
Jaspreet Kaur ◽  
Trishni Putty ◽  
Alex Quach ◽  
...  
Keyword(s):  
Vitamin D ◽  
Innate Immunity ◽  
Surface Expression ◽  
Microbial Pathogens ◽  
Cell Surface Expression ◽  
Complement Receptor ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Multistep Process ◽  
25 Hydroxyvitamin D

AbstractVitamin D deficiency remains a global concern. This ‘sunshine’ vitamin is converted through a multistep process to active 1,25-dihydroxyvitamin D3 (1,25D), the final step of which can occur in macrophages. Here we demonstrate a role for vitamin D in innate immunity. The expression of the complement receptor immunoglobulin (CRIg), which plays an important role in innate immunity, is upregulated by 1,25D in human macrophages. Monocytes cultured in 1,25D differentiated into macrophages displaying increased CRIg mRNA, protein and cell surface expression but not in classical complement receptors, CR3 and CR4. This was associated with increases in phagocytosis of complement opsonised Staphylococcus aureus and Candida albicans. Treating macrophages with 1,25D for 24 h also increases CRIg expression. While treating macrophages with 25-hydroxyvitamin D3 does not increase CRIg expression, added together with the toll like receptor 2 agonist, triacylated lipopeptide, Pam3CSK4, which promotes the conversion of 25-hydroxyvitamin D3 to 1,25D, leads to an increase in CRIg expression and increases in CYP27B1 mRNA. These findings suggest that macrophages harbour a vitamin D-primed innate defence mechanism, involving CRIg.

scholarly journals Immunological Aspects of SARS-CoV-2 Infection and the Putative Beneficial Role of Vitamin-D

2021 ◽  
Vol 22 (10) ◽  
pp. 5251
Author(s):  
Ming-Yieh Peng ◽  
Wen-Chih Liu ◽  
Jing-Quan Zheng ◽  
Chien-Lin Lu ◽  
Yi-Chou Hou ◽  
...  
Keyword(s):  
Vitamin D ◽  
Innate Immunity ◽  
T Cells ◽  
Adaptive Immunity ◽  
Cd4 T Cells ◽  
Vitamin D Supplementation ◽  
The Body ◽  
Alveolar Type ◽  
Tissue Destruction ◽  
Health Crisis

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is still an ongoing global health crisis. Immediately after the inhalation of SARS-CoV-2 viral particles, alveolar type II epithelial cells harbor and initiate local innate immunity. These particles can infect circulating macrophages, which then present the coronavirus antigens to T cells. Subsequently, the activation and differentiation of various types of T cells, as well as uncontrollable cytokine release (also known as cytokine storms), result in tissue destruction and amplification of the immune response. Vitamin D enhances the innate immunity required for combating COVID-19 by activating toll-like receptor 2. It also enhances antimicrobial peptide synthesis, such as through the promotion of the expression and secretion of cathelicidin and β-defensin; promotes autophagy through autophagosome formation; and increases the synthesis of lysosomal degradation enzymes within macrophages. Regarding adaptive immunity, vitamin D enhances CD4+ T cells, suppresses T helper 17 cells, and promotes the production of virus-specific antibodies by activating T cell-dependent B cells. Moreover, vitamin D attenuates the release of pro-inflammatory cytokines by CD4+ T cells through nuclear factor κB signaling, thereby inhibiting the development of a cytokine storm. SARS-CoV-2 enters cells after its spike proteins are bound to angiotensin-converting enzyme 2 (ACE2) receptors. Vitamin D increases the bioavailability and expression of ACE2, which may be responsible for trapping and inactivating the virus. Activation of the renin–angiotensin–aldosterone system (RAS) is responsible for tissue destruction, inflammation, and organ failure related to SARS-CoV-2. Vitamin D inhibits renin expression and serves as a negative RAS regulator. In conclusion, vitamin D defends the body against SARS-CoV-2 through a novel complex mechanism that operates through interactions between the activation of both innate and adaptive immunity, ACE2 expression, and inhibition of the RAS system. Multiple observation studies have shown that serum concentrations of 25 hydroxyvitamin D are inversely correlated with the incidence or severity of COVID-19. The evidence gathered thus far, generally meets Hill’s causality criteria in a biological system, although experimental verification is not sufficient. We speculated that adequate vitamin D supplementation may be essential for mitigating the progression and severity of COVID-19. Future studies are warranted to determine the dosage and effectiveness of vitamin D supplementation among different populations of individuals with COVID-19.

scholarly journals P1-345: Role of Vitamin D Signaling in Sporadic Alzheimer’s Disease: A Clinico-Experimental Study

2016 ◽  
Vol 12 ◽  
pp. P561-P562
Author(s):  
Anindita Banerjee ◽  
Vineet Kumar Khemka ◽  
Debashree Roy ◽  
Aparajita Dhar ◽  
Tapan Kumar Sinha Roy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Experimental Study ◽  
Vitamin D ◽  
Sporadic Alzheimer’S Disease ◽  
Vitamin D Signaling

scholarly journals Back to the future: a new look at ‘old’ vitamin D

2008 ◽  
Vol 198 (2) ◽  
pp. 261-269 ◽  
Author(s):  
Rene F Chun ◽  
John S Adams ◽  
Martin Hewison
Keyword(s):  
Vitamin D ◽  
Vitamin D Insufficiency ◽  
Target Cells ◽  
Bone Homeostasis ◽  
Immune Disorders ◽  
Factors Associated ◽  
Dihydroxyvitamin D ◽  
High Prevalence ◽  
Fresh Perspective ◽  
Vitamin D Signaling

Our perception of the vitamin D system continues to evolve. Recent studies have re-evaluated the parameters for adequate vitamin D status in humans, revealing a high prevalence of insufficiency in many populations throughout the world. Other reports have highlighted the potential consequences of vitamin D insufficiency beyond established effects on bone homeostasis. Most notably, there is now strong evidence of a role for vitamin D in modulating innate and adaptive immunities, with insufficiency being linked to infectious disease and other immune disorders. To date, signaling pathways for these new responses to vitamin D have been based on established endocrine models for active 1,25-dihydroxyvitamin D, despite present evidence for more localized, intracrine modes of action. In the following review, we provide a fresh perspective on vitamin D signaling in non-classical target cells such as macrophages by highlighting novel factors associated with the transport and action of this pluripotent secosteroid.

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