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Vitamin D deficiency in association with endothelial dysfunction: Implications for patients with COVID-19.
Zhang, J, McCullough, PA, Tecson, KM
Reviews in cardiovascular medicine. 2020;(3):339-344
Abstract
There is emerging evidence to suggest that vitamin D deficiency is associated with adverse outcomes in COVID-19 patients. Conversely, vitamin D supplementation protects against an initial alveolar diffuse damage of COVID-19 becoming progressively worse. The mechanisms by which vitamin D deficiency exacerbates COVID-19 pneumonia remain poorly understood. In this review we describe the rationale of the putative role of endothelial dysfunction in this event. Herein, we will briefly review (1) anti-inflammatory and anti-thrombotic effects of vitamin D, (2) vitamin D receptor and vitamin D receptor ligand, (3) protective role of vitamin D against endothelial dysfunction, (4) risk of vitamin D deficiency, (5) vitamin D deficiency in association with endothelial dysfunction, (6) the characteristics of vitamin D relevant to COVID-19, (7) the role of vitamin D on innate and adaptive response, (8) biomarkers of endothelial cell activation contributing to cytokine storm, and (9) the bidirectional relationship between inflammation and homeostasis. Finally, we hypothesize that endothelial dysfunction relevant to vitamin D deficiency results from decreased binding of the vitamin D receptor with its ligand on the vascular endothelium and that it may be immune-mediated via increased interferon 1 α. A possible sequence of events may be described as (1) angiotensin II converting enzyme-related initial endothelial injury followed by vitamin D receptor-related endothelial dysfunction, (2) endothelial lesions deteriorating to endothelialitis, coagulopathy and thrombosis, and (3) vascular damage exacerbating pulmonary pathology and making patients with vitamin D deficiency vulnerable to death.
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Substantial Variability Across Individuals in the Vascular and Nutrigenomic Response to an Acute Intake of Curcumin: A Randomized Controlled Trial.
Barber-Chamoux, N, Milenkovic, D, Verny, MA, Habauzit, V, Pereira, B, Lambert, C, Richard, D, Boby, C, Mazur, A, Lusson, JR, et al
Molecular nutrition & food research. 2018;(5)
Abstract
SCOPE Curcumin exerts biological activities of interest in cardiovascular prevention. However, its vascular protective effect is still poorly investigated in humans. The present study aims to assess vascular effect of an acute intake of curcumin and its nutrigenomic impact in circulating immune cells. METHODS AND RESULTS In a randomized, double-blind, crossover design, 18 healthy smokers consume a placebo or a 5-g curcumin. Before and 2 h after the intake, vascular function measurements are performed by using flow-mediated dilation (FMD). In addition, endothelial function in the microcirculation and blood pressure are evaluated. Plasma curcumin concentrations and changes in gene expression in peripheral blood mononuclear cells (PBMC) are analyzed. No significant effect of curcumin on FMD is observed when considering the entire study population, mainly due to a high interindividual variability. A subgroup analysis according to the gender or the cardiovascular-risk score reveals a significant effect of curcumin on FMD in women and in subjects presenting lower cardiovascular risk. No change in gene expression is observed when data are analyzed for all volunteers but changes in expression are observed when analyzed according to gender. CONCLUSIONS This clinical trial highlights that a substantial variability in efficacy of curcumin exists across individuals.
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High-Density Lipoproteins: Effects on Vascular Function and Role in the Immune Response.
Haghikia, A, Landmesser, U
Cardiology clinics. 2018;(2):317-327
Abstract
The focus in studies of high-density lipoproteins was on their capacity to remove excess cholesterol and deliver it to the liver. Other functions and vascular effects have been described. Clinical trials and translational/genetic studies have led to a refined understanding of the role of high-density lipoprotein; it is likely not a causal cardiovascular risk factor. In healthy subjects, it limits lipid oxidation, protects endothelial cell functions/integrity, and exerts antiinflammatory/antiapoptotic effects. In patients with coronary disease or diabetes, it undergoes modifications/remodeling, resulting in dysfunctional high-density lipoprotein. We summarize recent findings about the regulation of its function and discuss the clinical implications.
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Enhancing capillary blood collection: The influence of nicotinic acid and nonivamide.
Moro, C, Bass, J, Scott, AM, Canetti, EFD
Journal of clinical laboratory analysis. 2017;(6)
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Abstract
BACKGROUND Nicotinic acid and nonivamide are often applied topically during capillary blood collection to induce vasodilation. These molecules may have an influence on immune effector cell activity in nearby tissues. This study investigates whether the induction of flushing by nicotinic acid and nonivamide causes an inflammatory response that influences the composition of immune cells present in a capillary blood sample. METHODS Females aged between 18 and 30 years old provided capillary blood samples. Experimental samples were taken from an earlobe treated with nicotinic acid and nonivamide with controls obtained from the untreated earlobe. Immunophenotypic analyses were conducted using polychromatic flow cytometry to determine whether any changes occurred in leucocyte subpopulations (CD3, CD4, CD8, CD19, CD56, and CD14) and granulocytic functional-related surface antigen markers (CD11b, CD18, CD16b, and CD66b). RESULTS No significant differences were observed between experimental and control samples in the mean percent of parent for the lymphocyte, monocyte, or granulocyte subpopulations, or in the median fluorescence intensity of particular surface markers expressed on these leucocytes. CONCLUSION The topical application of nicotinic acid and nonivamide is a possible method to improve capillary blood collection for immunological assessments. The use of these agents may increase the safety and compliance of patients who suffer from needle phobia or are unable to provide venous blood samples.
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Hydrocortisone and Ascorbic Acid Synergistically Prevent and Repair Lipopolysaccharide-Induced Pulmonary Endothelial Barrier Dysfunction.
Barabutis, N, Khangoora, V, Marik, PE, Catravas, JD
Chest. 2017;(5):954-962
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Abstract
BACKGROUND Sepsis refers to the dysregulated host immune response elicited by microbial infections resulting in life-threatening organ dysfunction. Sepsis represents a medical challenge, since it is associated with a rate of death as high as 60%. Septic shock is strongly associated with vascular dysfunction and elevated pulmonary capillary permeability. We recently reported that the combination of hydrocortisone (HC), ascorbic acid (vitC), and thiamine dramatically improves outcomes and reduces mortality in patients with sepsis. In the present study, we provide experimental evidence in support of the hypothesis that the combination of HC and vitC enhances endothelial barrier function. METHODS Human lung microvascular endothelial cells were exposed to lipopolysaccharide (LPS) in the absence or presence of HC and vitC. RESULTS LPS alone induced profound hyperpermeability, as reflected in decreased values of transendothelial electrical resistance. vitC alone did not exhibit barrier enhancement properties nor did it affect the LPS-induced hyperpermeability. Similarly, HC alone exhibited only a minor barrier-enhancing and protective effect. Conversely, the combination of HC and vitC, either as before or after treatment, dramatically reversed the LPS-induced barrier dysfunction. The barrier-protective effects of HC and vitC were associated with reversal of LPS-induced p53 and phosphorylated cofilin downregulation and LPS-induced RhoA activation and myosin light chain phosphorylation. CONCLUSIONS These data provide a novel mechanism of endothelial barrier protection and suggest one possible pathway that may contribute to the therapeutic effects of HC and vitC in patients with sepsis.