Vitamin D supplementation, bone turnover, and inflammation in HIV-infected patients

Benguella, L.; Arbault, Anaïs; Fillion, Anne; Blot, Mathieu; Piroth, C.; Denimal, Damien; Duvillard, Laurence; Ornetti, Paul; Chavanet, P.; Maillefert, Jean-Françis; Piroth, Lionel

doi:10.1016/j.medmal.2018.02.011

Cited by 10 publications

(4 citation statements)

References 33 publications

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“…In inflammatory bowel disease (IBD) and chronic kidney disease (CKD), vitamin D treatment has been associated with reduced levels of systemic inflammation and disease activity [45,46,47]. However, similar to our results, vitamin D supplementation did not modulate systemic immune activation in HIV-1, or in obesity studies [48,49,50]. PBA is a histone deacetylase (HDAC) inhibitor, and a synthetic analogue to the short-chain fatty acid (SCFA) butyrate.…”

Section: Discussionsupporting

confidence: 82%

Vitamin D and Phenylbutyrate Supplementation Does Not Modulate Gut Derived Immune Activation in HIV-1

et al. 2019

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Dysbiosis and a dysregulated gut immune barrier function contributes to chronic immune activation in HIV-1 infection. We investigated if nutritional supplementation with vitamin D and phenylbutyrate could improve gut-derived inflammation, selected microbial metabolites, and composition of the gut microbiota. Treatment-naïve HIV-1-infected individuals (n = 167) were included from a double-blind, randomized, and placebo-controlled trial of daily 5000 IU vitamin D and 500 mg phenylbutyrate for 16 weeks (Clinicaltrials.gov NCT01702974). Baseline and per-protocol plasma samples at week 16 were analysed for soluble CD14, the antimicrobial peptide LL-37, kynurenine/tryptophan-ratio, TMAO, choline, and betaine. Assessment of the gut microbiota involved 16S rRNA gene sequencing of colonic biopsies. Vitamin D + phenylbutyrate treatment significantly increased 25-hydroxyvitamin D levels (p < 0.001) but had no effects on sCD14, the kynurenine/tryptophan-ratio, TMAO, or choline levels. Subgroup-analyses of vitamin D insufficient subjects demonstrated a significant increase of LL-37 in the treatment group (p = 0.02), whereas treatment failed to significantly impact LL-37-levels in multiple regression analysis. Further, no effects on the microbiota was found in number of operational taxonomic units (p = 0.71), Shannon microbial diversity index (p = 0.82), or in principal component analyses (p = 0.83). Nutritional supplementation with vitamin D + phenylbutyrate did not modulate gut-derived inflammatory markers or microbial composition in treatment-naïve HIV-1 individuals with active viral replication.

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Section: Discussionsupporting

confidence: 82%

Vitamin D and Phenylbutyrate Supplementation Does Not Modulate Gut Derived Immune Activation in HIV-1

et al. 2019

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“…The inhibitory effect of vitamin D/VDR signaling on inflammatory diseases, including inflammatory bowel diseases and HIV-infected disorders, has been reported in previous investigations (16,39). We first showed that vitamin D plays a protective role in OLP in 2017 (18), but the mechanism whereby vitamin D inhibits OLP development remains unclear.…”

Section: Discussionmentioning

confidence: 80%

Vitamin D/VDR signaling suppresses microRNA‐802‐induced apoptosis of keratinocytes in oral lichen planus

Zhao

et al. 2018

The FASEB Journal

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Vitamin D is known to play a protective role in inflammatory diseases. Although the suppressive effect of vitamin D/vitamin D receptor (VDR) signaling has been shown in the context of oral lichen planus (OLP), the molecular basis of its regulatory function remains poorly understood. Herein, we reported that miR-802 overexpression in OLP could aggravate apoptosis of oral keratinocytes by targeting B-cell lymphoma 2 mRNA. In addition, vitamin D/VDR signaling was able to suppress miR-802 expression in LPS-treated or activated CD4 T cell-stimulated human oral keratinocytes by blocking NF-κB pathways, thereby inhibiting OLP apoptosis. Consistent with the results in vitro, we showed that miR-802 expression was enhanced in oral keratinocytes from VDR mice, and an inverse correlation between VDR and miR-802 was found in human biopsy specimens of OLP. Collectively, our data suggest that vitamin D/VDR signaling suppresses oral keratinocyte apoptosis by targeting miR-802.-Zhao, B., Xu, N., Li, R., Yu, F., Zhang, F., Yang, F., Ge, X., Li, Y. C., Du, J. Vitamin D/VDR signaling suppresses microRNA-802-induced apoptosis of keratinocytes in oral lichen planus.

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“…We excluded case reports, studies with <15 individuals, studies which supplemented with several micronutrients at once or did not report on VitD supplementation, as well as those that were conducted in a non-HIV population. In addition, to control for variability, a supplementation trial was also excluded due to low patient adherence (18).…”

Section: Introductionmentioning

confidence: 99%

The Potential Protective Role of Vitamin D Supplementation on HIV-1 Infection

2019

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HIV infection remains a global and public health issue with the incidence increasing in some countries. Despite the fact that combination antiretroviral therapy (cART) has decreased mortality and increased the life expectancy of HIV-infected individuals, non-AIDS conditions, mainly those associated with a persistent inflammatory state, have emerged as important causes of morbidity, and mortality despite effective antiviral therapy. One of the most common comorbidities in HIV-1 patients is Vitamin D (VitD) insufficiency, as VitD is a hormone that, in addition to its physiological role in mineral metabolism, has pleiotropic effects on immune regulation. Several reports have shown that VitD levels decrease during HIV disease progression and correlate with decreased survival rates, highlighting the importance of VitD supplementation during infection. An extensive review of 29 clinical studies of VitD supplementation in HIV-infected patients showed that regardless of cART, when VitD levels were increased to normal ranges, there was a decrease in inflammation, markers associated with bone turnover, and the risk of secondary hyperparathyroidism while the anti-bacterial response was increased. Additionally, in 3 of 7 studies, VitD supplementation led to an increase in CD4+ T cell count, although its effect on viral load was inconclusive since most patients were on cART. Similarly, previous evidence from our laboratory has shown that VitD can reduce the infection of CD4+ T cells in vitro. The effect of VitD supplementation on other HIV-associated conditions, such as cardiovascular diseases, dyslipidemia or hypertension, warrants further exploration. Currently, the available evidence suggests that there is a potential role for VitD supplementation in people living with HIV-1, however, comprehensive studies are required to define an adequate supplementation protocol for these individuals.

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Vitamin D supplementation, bone turnover, and inflammation in HIV-infected patients

Cited by 10 publications

References 33 publications

Vitamin D and Phenylbutyrate Supplementation Does Not Modulate Gut Derived Immune Activation in HIV-1

Vitamin D and Phenylbutyrate Supplementation Does Not Modulate Gut Derived Immune Activation in HIV-1

Vitamin D/VDR signaling suppresses microRNA‐802‐induced apoptosis of keratinocytes in oral lichen planus

The Potential Protective Role of Vitamin D Supplementation on HIV-1 Infection

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