1,25-dihydroxyvitamin D 3 down-modulates the production of proinflammatory cytokines and nitric oxide and enhances the phosphorylation of monocyte-expressed STAT6 at the recent-onset type 1 diabetes

Ysmail-Dahlouk, Lamia; Nouari, Wafa; Aribi, Mourad

doi:10.1016/j.imlet.2016.10.002

Cited by 26 publications

(13 citation statements)

References 61 publications

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“…51,52 The levels of various cytokines in the DRs underscore a trend of Th cell polarization toward a particular subset but do not directly reflect accurate cell polarization counts. As several studies have shown the generation of FoxP3+ CD4 + T cells from peripheral blood in response to calcitriol intervention, 51 [56][57][58] Available data also demonstrate that calcitriol promotes the development of Th2 cells to positively regulate IL-4, IL-5, and IL-10 production and prevent strong Th1 responses in immune diseases. 59,60 These findings are consistent with our results from rat peripheral blood samples.…”

Section: Discussionmentioning

confidence: 95%

“…Our data showed that calcitriol intervention could skew Th1, Th17, Th2, and Treg polarization phenotypes from a predominance of Th1 and Th17 cells toward a predominance of Th2 and Treg cells in LPS‐induced periodontitis. The suppressive effects of calcitriol on the immune response are largely characterized by the inhibition of Th1 proliferation and the promotion of IL‐10 release . Available data also demonstrate that calcitriol promotes the development of Th2 cells to positively regulate IL‐4, IL‐5, and IL‐10 production and prevent strong Th1 responses in immune diseases .…”

Section: Discussionmentioning

confidence: 99%

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Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Wang

et al. 2019

J of Periodontal Research

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Background Although the immunomodulatory properties of calcitriol in bone metabolism have been documented for decades, its therapeutic role in the management of periodontitis remains largely unexplored. In this study, we hypothesized that calcitriol suppresses lipopolysaccharide (LPS)‐induced alveolar bone loss by regulating T helper (Th) cell subset polarization. Methods To test this hypothesis, we determined the effect of calcitriol intervention on the development of LPS‐induced periodontitis in rats in terms of bone loss (micro‐CT analysis), local inflammatory infiltration levels, the number of osteoclasts (hematoxylin and eosin staining) and the level of osteoclastogenesis (tartrate‐resistant acid phosphatase method). Furthermore, immunohistochemistry was used to assess the expression levels of the receptor activator of NF‐κB ligand (RANKL) and osteoprotegerin (OPG) as well as the cytokine levels of interferon‐γ (IFN‐γ), interleukin‐4 (IL‐4), IL‐17, and IL‐10 throughout the LPS‐injected region. Finally, the polarization potential of Th cells in peripheral blood was analyzed using flow cytometry. Results Calcitriol intervention decreased alveolar bone loss in response to LPS injection and inflammatory cell infiltration. Analysis of osteoclast number and RANKL and OPG expression showed that bone resorption activity was largely suppressed in response to calcitriol administration, along with decreased IL‐17 levels but increased IL‐4 and IL‐10 levels in periodontal tissues (the LPS‐injected region). Similarly, the percentages of Th2 and Treg cells in peripheral blood increased, but the percentages of Th1 and Th17 cells decreased in rats receiving calcitriol. Conclusion Our findings suggest that calcitriol can be used to inhibit bone loss in experimental periodontitis, likely via the regulation of local and systemic Th cell polarization.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Wang

et al. 2019

J of Periodontal Research

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“…In pancreatic islets, 1,25(OH) 2 D decreases, as was shown in in vitro and in vivo experiments, the expression of pro-inflammatory cytokines (e.g., IL-6), which are involved in the pathogenesis of T1D, making β-cells less chemoattractive and less prone to inflammation [14]. This leads to a decrease in T-cell recruitment and infiltration, an increase in regulatory cells, and a delay in the autoimmune process.…”

Section: Vitamin D In Maintaining Pancreatic β-Cell Function and Regumentioning

confidence: 65%

“…This leads to a decrease in T-cell recruitment and infiltration, an increase in regulatory cells, and a delay in the autoimmune process. In addition, 1,25(OH) 2 D reduces the expression of MHC class I, leading to a decrease in the vulnerability of islet β-cells to the action of cytotoxic T lymphocytes [13,14].…”

Section: Vitamin D In Maintaining Pancreatic β-Cell Function and Regumentioning

confidence: 99%

Vitamin D Deficiency and Diabetes Mellitus

Shymanskyi¹,

Lisakovska²,

Mazanova³

et al. 2020

Vitamin D Deficiency

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Vitamin D (VD) is a molecule that can be synthesized directly in the humans' body or enter the organism with food in the form of inactive precursors. To exert its biological action, VD undergoes two-stage hydroxylation (at the 25th and 1st position) catalyzed by cytochromes P450, the presence of which has already been shown in almost all tissues of the human body. The product of hydroxylation is hormone-active form of vitamin D-1,25(OH) 2 D. 1,25(OH) 2 D binds to specific vitamin D receptor (VDR) and regulates the expression of genes involved in bone remodeling (classical function) and genes that control immune response, hormone secretion, cell proliferation, and differentiation (nonclassical functions). VD deficiency is prevalent around the globe and may be one of the key factors for diabetes development. The direct association between vitamin D deficiency and type 1 (T1D) and type 2 (T2D) diabetes has been proven. Detection of VDR in pancreas and adipose tissue, skeletal muscles, and immune cells allowed implying the antidiabetic role of vitamin D by enhancing insulin synthesis and exocytosis, increasing the expression of the insulin receptor, and modulating immune cells' functions. This chapter summarizes data about relationship between VD insufficiency/deficiency and development of T1D and T2D, and their complications.

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“…[20,21] A highly significant relationship is demonstrated between insufficient sleep and frequent mental distress (FMD), also between FMD and chronic disease. [22,23] In addition, considerable data proposed that chronic mental distress can lead to changes in appetite-regulating hormones and insulin resistance. The former conditions can further develop into chronic metabolic impairments like diabetes.…”

Section: Discussionmentioning

confidence: 99%

Emotional exhaustion-induced latent autoimmune diabetes in adults in a young lady

et al. 2017

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Rationale:Latent autoimmune diabetes in adults (LADA) refers to an autoimmune disorder characterized with detectable islets antibodies in the early diagnosis and increased autoimmune beta-cell failure progression. Notably, this kind of diabetes seems to be confused with other phenotypic diabetes.Patient concerns:A young woman suffered an emotional exhaustion-induced LADA, showing asthenia, polydipsia, polyuria, and visible weight loss. The patient emotionally ended a 14-year romantic relationship, leading to the emotional flooding.Diagnoses:The data from physical examination and laboratory tests exhibited as follows: glutamic acid decarboxylase antibody (GADA) = 63.83 U/mL, the fasting blood glucose (FBG) = 13.3 mmol/L, and glycated haemoglobin (HbA1c) = 10.9%. According to levels of GADA, the patient was diagnosed as LADA.Interventions:The patient was clinically treated with insulin for 3-month. Then, running, diet-control, and emotional treatment were combined, such as the patient started a new relationship.Outcomes:An emotional recovery initiated from a new romantic relationship and a baby, showing normal levels of GAD65 (27.007 IU/mL) and FBG (5.46) mmol/L.Lessons:The emotional exhaustion might play a significant role in induction of LADA. It is important that individuals should maintain optimism, cheer, and a positive attitude.

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1,25-dihydroxyvitamin D 3 down-modulates the production of proinflammatory cytokines and nitric oxide and enhances the phosphorylation of monocyte-expressed STAT6 at the recent-onset type 1 diabetes

Cited by 26 publications

References 61 publications

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Vitamin D Deficiency and Diabetes Mellitus

Emotional exhaustion-induced latent autoimmune diabetes in adults in a young lady

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