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PMID: 

Environ Sci Pollut Res Int. 2020 Mar 24. Epub 2020 Mar 24. PMID: 32212071

Abstract Title: 

Effect of mobile phone radiation on oxidative stress, inflammatory response, and contextual fear memory in Wistar rat.

Abstract: 

In the present lifestyle, we are continuously exposed to radiofrequency electromagnetic field (RF-EMF) radiation generated mainly by mobile phones (MP). Among other organs, our brain and hippocampus in specific, is the region where effect of any environmental perturbation is most pronounced. So, this study was aimed to examine changes in major parameters (oxidative stress, level of pro-inflammatory cytokines (PICs), hypothalamic-pituitary-adrenal (HPA) axis hormones, and contextual fear conditioning) which are linked to hippocampus directly or indirectly, upon exposure to mobile phone radiofrequency electromagnetic field (MP-RF-EMF) radiation. Exposure was performed on young adult male Wistar rats for 16 weeks continuously (2 h/day) with MP-RF-EMF radiation having frequency, power density, and specific absorption rate (SAR) of 1966.1 MHz, 4.0 mW/cm, and 0.36 W/kg, respectively. Another set of animals kept in similar conditions without any radiation exposure serves as control. Towards the end of exposure period, animals were tested for fear memory and then euthanized to measure hippocampal oxidative stress, level of circulatory PICs, and stress hormones. We observed significant increase in hippocampal oxidative stress (p 

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PMID: 

Zhonghua Nan Ke Xue. 2019 May ;25(5):451-455. PMID: 32216233

Abstract Title: 

[Impacts of electromagnetic radiation from cellphones and Wi-Fi on spermatogenesis].

Abstract: 

With the development of Wi-Fi technology and widespread exposure to electromagnetic radiation (EMR), people are increasingly concerned about the health hazards caused by radiofrequency electromagnetic fields as from cellphones and Wi-Fi, particularly about the current decline in sperm concentration and increase in male infertility. Long-term exposure to EMR not only damages male reproductive organs, but also affects the number, morphology, motility and oocyte-binding ability of sperm, and indirectly increases the risk of infertility. However, EMR is not unavoidable. Low-intensity short-term or intermittent exposure to EMR has little adverse effect on reproductive organs and sperm. And many antioxidant and anti-free radical agents, such as vitamin E and melatonin, can protect some special populations from EMR. This review presents an overview of the impacts of EMR from cellphones and Wi-Fi on sperm, some countermeasures, and prospects of EMR protection.

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PMID: 

J Periodontal Res. 2019 Apr ;54(2):154-163. Epub 2018 Oct 8. PMID: 30295316

Abstract Title: 

Vitamin D attenuates human gingival fibroblast inflammatory cytokine production following advanced glycation end product interaction with receptors for AGE.

Abstract: 

BACKGROUND AND OBJECTIVES: Vitamin D [1,25(OH)Dor 1,25D3] is critical in musculoskeletal health, inflammation, immune response, and glucose metabolism. Patients with vitamin D deficiency may be at higher risk of diabetes and periodontitis. Diabetic patients exhibit exacerbated inflammation and more periodontal destruction. Advanced glycation end products (AGEs), formed during diabetic hyperglycemia, activate inflammatory pathways in periodontitis. Human gingival fibroblasts (HGFs) express receptors for AGEs (RAGEs) and can contribute to inflammation.OBJECTIVES: Determine whether glycated human serum albumin (G-HSA) augments HGF IL-6 and IL-8 production, and whether treatment with 1,25D3 attenuates cytokine production following stimulation with G-HSA + IL-1β and/or IL-17.MATERIAL AND METHODS: HGFs were incubated±G-HSA or normal human serum albumin (HSA), ±IL-1β and/or IL-17, ±1,25D3. Cytokines were measured by ELISA. Neutralizing anti-RAGE was used to assess AGE-RAGE interaction. Endotoxin was measured using the ToxinSensor™ System. Data were expressed as mean ± standard deviation and analyzed using a one-way analysis of variance (ANOVA) and Scheffe's F procedure for post hoc comparisons.RESULTS: G-HSA or IL-1β, but not HSA, significantly stimulated IL-6 and IL-8 production. G-HSA or HSA when combined with IL-1β or IL-1β + IL-17 synergistically stimulated IL-6 and IL-8. Neutralizing anti-RAGE inhibited IL-6 and IL-8 produced by cells stimulated with IL-1β + G-HSA but not (+HSA). Synergism causedby HSA did not appear to be mediated by endotoxin since its levels in G-HSA and HSA were not sufficient to stimulate fibroblasts. Vitamin D inhibited IL-6 and IL-8 production stimulated by G-HSA or HSA + IL-1β or IL-1β + IL-17.CONCLUSIONS: Results suggest that the"perioprotective"effects of vitamin D are related to its ability to regulate inflammatory cytokine production by HGFs following AGE-RAGE interaction.

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PMID: 

Eur J Microbiol Immunol (Bp). 2019 Oct 3 ;9(3):80-87. Epub 2019 Aug 13. PMID: 31662886

Abstract Title: 

Antimicrobial and Immune-Modulatory Effects of Vitamin D Provide Promising Antibiotics-Independent Approaches to Tackle Bacterial Infections – Lessons Learnt from a Literature Survey.

Abstract: 

Antimicrobial multidrug-resistance (MDR) constitutes an emerging threat to global health and makes the effective prevention and treatment of many, particularly severe infections challenging, if not impossible. Many antibiotic classes have lost antimicrobial efficacy against a plethora of infectious agents including bacterial species due to microbial acquisition of distinct resistance genes. Hence, the development of novel anti-infectious intervention strategies including antibiotic-independent approaches is urgently needed. Vitamins such as vitamin D and vitamin D derivates might be such promising molecular candidates to combat infections caused by bacteria including MDR strains. Using the Pubmed database, we therefore performed an in-depth literature survey, searching for publications on the antimicrobial effect of vitamin D directed against bacteria including MDR strains. In vitro and clinical studies between 2009 and 2019 revealed that vitamin D does, in fact, possess antimicrobial properties against both Gram-positive and Gram-negative bacterial species, whereas conflicting results could be obtained from in vivo studies. Taken together, the potential anti-infectious effects for the antibiotic-independent application of vitamin D and/or an adjunct therapy in combination with antibiotic compounds directed against infectious diseases such as tuberculosis,infections, or skin diseases, for instance, should be considered and further investigated in more detail.

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PMID: 

Burns Trauma. 2018 ;6:11. Epub 2018 Apr 16. PMID: 29721511

Abstract Title: 

Vitamin D status and its influence on outcomes following major burn injury and critical illness.

Abstract: 

Vitamin D deficiency is common among the general population. It is also observed in up to 76% of critically ill patients. Despite the high prevalence of hypovitaminosis D in critical illness, vitamin D is often overlooked by medical staff as the clinical implications and consequences of vitamin D deficiency in acute contexts remain to be fully understood. Vitamin D has a broad range of pleotropic effects on various processes and systems including the immune-inflammatory response. 1α,25-dihydroxyvitamin D (1,25(OH)D), has been shown to promote a tolerogenic immune response limiting deleterious inflammatory effects, modulation of the innate immune system, and enhancement of anti-microbial peptides. Vitamin D deficiency is frequently observed in critically ill patients and has been related to extrinsic causes (i.e., limited sunlight exposure), magnitude of injury/illness, or the treatment started by medical doctors including fluid resuscitation. Low levels of vitamin D in critically ill patients have been associated with sepsis, organ failure, and mortality. Despite this, there are subpopulations of critical illness, such as burn patients, where the literature regarding vitamin D status and its influence on outcomes remain insufficient. Thermal injury results in damage to both burned and non-burned tissues, as well as induces an exaggerated and persistent immune-inflammatory and hypermetabolic response. In this review, we propose potential mechanisms in which burn injury affects the vitamin D status and summarizes current literature investigating the influence of vitamin D status on outcomes. In addition, we reviewed the literature and trials investigating vitamin D supplementation in critically ill patients and discuss the therapeutic potential of vitamin D supplementation in burn and critically ill patients. We also highlight current limitations of studies that have investigated vitamin D status and supplementation in critical illness. Thermal injury influences vitamin D status. More studies investigating vitamin D depletion in burn patients and its influence on prognosis, via standardized methodology, are required to reach definitive conclusions and influence clinical practice.

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PMID: 

JCI Insight. 2018 09 6 ;3(17). Epub 2018 Sep 6. PMID: 30185660

Abstract Title: 

1,25-Dihydroxyvitamin D suppresses M1 macrophages and promotes M2 differentiation at bone injury sites.

Abstract: 

An indispensable role of macrophages in bone repair has been well recognized. Previous data have demonstrated the copresence of M1 macrophages and mesenchymal stem cells (MSCs) during the proinflammatory stage of bone repair. However, the exact role of M1 macrophages in MSC function and bone repair is unknown. This study aimed to define the role of M1 macrophages at bone injury sites via the function of 1,25-Dihydroxyvitamin D (1,25[OH]2D) in suppressing M1 but promoting M2 differentiation. We showed that 1,25(OH)2D suppressed M1 macrophage-mediated enhancement of MSC migration. Additionally, 1,25(OH)2D inhibited M1 macrophage secretion of osteogenic proteins (i.e., Oncostatin M, TNF-α, and IL-6). Importantly, the 1,25(OH)2D-mediated suppression of osteogenic function in M1 macrophages at the proinflammatory stage was associated with 1,25(OH)2D-mediated reduction of MSC abundance, compromised osteogenic potential of MSCs, and impairment of fracture repair. Furthermore, outsidethe proinflammatory stage, 1,25(OH)2D treatment did not suppress fracture repair. Accordingly, our data support 2 conclusions: (a) M1 macrophages are important for the recruitment and osteogenic priming of MSCs and, hence, are necessary for fracture repair, and (b) under vitamin D-sufficient conditions, 1,25(OH)2D treatment is unnecessary and can be detrimental if provided during the proinflammatory stage of fracture healing.

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PMID: 

Comp Immunol Microbiol Infect Dis. 2018 Aug ;59:17-23. Epub 2018 Sep 11. PMID: 30290883

Abstract Title: 

Calcitriol increases nitric oxide production and modulates microbicidal capacity against Mycobacterium bovis in bovine macrophages.

Abstract: 

Bovine tuberculosis, a re-emerging infectious disease caused by Mycobacterium bovis, can be transmitted to humans. Global prevalence of M. bovis in humans is underestimated and represents a serious public health risk in developing countries. In light of this situation, it is important to note that our understanding of the immunopathogenesis of human tuberculosis can be improved by studying this disease in the bovine model. Stimulation of the bovine innate immune system with calcitriol (1,25(OH)2D3) leads to an increase in bactericidal molecules involved in macrophage antimicrobial activity. It is unknown, however, if calcitriol´s effect on bovine macrophages impacts intracellular bacterial replication. With these considerations in mind, this study sought to investigate the specific role of calcitriol in tuberculosis control in bovine macrophages, in the hopes of uncovering information applicable to human tuberculosis. Assuch, infection with M. bovis was shown to induce expression of CYP27B1 and VDR genes in macrophages. Moreover, addition of 1,25(OH)2D3 to cultures of macrophages previously infected with mycobacteria and/or activated by LPS triggered cellular expression of nitric oxide synthase (NOS2) and increased nitrite concentrations, both indicators of nitric oxide (NO) production. By means of a microbicidal assay, addition of 1,25(OH)2D3 was seen to increase macrophage phagocytosis and to decrease mycobacterial intracellular replication. Thus, taken together, our results show that calcitriol can help stimulate the innate immune system of bovines by increasing phagocytosis and decreasing intracellular replication of microorganisms, such as M. bovis, in macrophages, through the VDR pathway.

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PMID: 

PLoS One. 2019 ;14(4):e0215383. Epub 2019 Apr 12. PMID: 30978243

Abstract Title: 

25(OH)D3 and 1.25(OH)2D3 inhibits TNF-α expression in human monocyte derived macrophages.

Abstract: 

PURPOSE: We wanted to investigate effects of vitamin D3 (25(OH)D3 and 1.25(OH)2D3) on inflammatory cytokine expression in both activated and non-activated Mφ.MATERIALS AND METHODS: Mononuclear cells, isolated from healthy donor buffy coats were cultured for a 6-day differentiation-period. Fully differentiated Mφ were pre-treated with either 25(OH)D3 or 1.25(OH)2D3 for (4, 12 or 24 hours) +/-LPS challenge for 4 hours. Gene expression analyses of VDR, Cyp27b1 and pro-inflammatory markers TNF-α, IL-6, NF-κB, MCP-1, was performed using RT-quantitative PCR. TNF-α protein levels from Mφ culture media wereanalysed by ELISA.RESULTS: Both 25(OH)D3 and 1.25(OH)2D3 significantly inhibited TNF-α expression in both LPS-stimulated and unstimulated Mφ. Also, NF-κB, and to a lesser extend IL-6 and MCP-1 were inhibited. LPS up-regulated Cyp27b1 gene expression which was partly reverted by 1.25(OH)2D3.CONCLUSION: These data show anti-inflammatory effects of vitamin D3 (25(OH)D3 and 1.25(OH)2D3) in human macrophages, and support, that means for targeting high dose vitamin D3 to the immune system may have beneficial clinical effect in inflammatory conditions.

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PMID: 

Nutrients. 2019 May 7 ;11(5). Epub 2019 May 7. PMID: 31067701

Abstract Title: 

The Role of Vitamin D in Inflammatory Bowel Disease: Mechanism to Management.

Abstract: 

Vitamin D has been linked to human health benefits that extend far beyond its established actions on calcium homeostasis and bone metabolism. One of the most well studied facets of extra-skeletal vitamin D is its activity as an immuno-modulator, in particular its potent anti-inflammatory effects. As a consequence, vitamin D deficiency has been associated with inflammatory diseases including inflammatory bowel disease (IBD). Low serum levels of the major circulating form of vitamin D, 25-hydroxyvitamin D (25-OH-D) are significantly more prevalent in patients with IBD, particularly in the winter and spring months when UV-induced synthesis of vitamin D is lower. Dietary malabsorption of vitamin D may also contribute to low serum 25(OH)D in IBD. The benefits of supplementation with vitamin D for IBD patients are still unclear, and improved vitamin D status may help to prevent the onset of IBD as well as ameliorating disease severity. Beneficial effects of vitamin D in IBD are supported by pre-clinical studies, notably with mouse models, where the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH)2D) has been shown to regulate gastrointestinal microbiota function, and promote anti-inflammatory, tolerogenic immune responses. The current narrative review aims to summarise the different strands of data linking vitamin D and IBD, whilst also outlining the possible beneficial effects of vitamin D supplementation in managing IBD in humans.

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