Vitamin D receptor stimulation to reduce acute respiratory distress syndrome (ARDS) in patients with coronavirus SARS-CoV-2 infections: Revised Ms SBMB 2020_166

Jose Manuel Quesada-Gomez, Marta Entrenas-Castillo, Roger Bouillon, Jose Manuel Quesada-Gomez, Marta Entrenas-Castillo, Roger Bouillon

Abstract

Coronavirus infection is a serious health problem awaiting an effective vaccine and/or antiviral treatment. The major complication of coronavirus disease 2019 (COVID-19), the Acute Respiratory Distress syndrome (ARDS), is due to a variety of mechanisms including cytokine storm, dysregulation of the renin-angiotensin system, neutrophil activation and increased (micro)coagulation. Based on many preclinical studies and observational data in humans, ARDS may be aggravated by vitamin D deficiency and tapered down by activation of the vitamin D receptor. Several randomized clinical trials using either oral vitamin D or oral Calcifediol (25OHD) are ongoing. Based on a pilot study, oral calcifediol may be the most promising approach. These studies are expected to provide guidelines within a few months.

Keywords: 1α, 25(OH)2D or 1α, 25-dihydroxyvitamin D or calcitriol; Acute respiratory distress syndrome (ARDS); Calcifediol or 25-hydroxyvitamin D3; Corona virus; Cytokine storm; Hypercoagulability; Lung diseases; Renin-angiotensin system; SARS-CoV-2; Vitamin D, vitamin D3 or cholecalciferol.

Copyright © 2020 Elsevier Ltd. All rights reserved.

Figures

Fig. 1
Fig. 1
The mechanisms involved in the pathogenesis of Acute Respiratory Distress Syndrome (ARDS) including cytokine and chemokine storm (release of large amounts by immune effector cells), Excessive activation and recruitment of neutrophils into inflamed interstitium and alveolar space with disruption of the endothelial-epithelial barrier and alveolar damage, and dysregulation of the coagulation cascade generating intra-alveolar or systemic fibrin clots and thrombotic complications. The vitamin D endocrine system minimizes ARDS. The vitamin D receptor (VDR) and enzymes of the vitamin D endocrine system are expressed in the cuboidal alveolar type II cells (ACII) and monocyte/macrophages and activated lymphocytes. The availability of calcifediol is critical for synthesizing calcitriol, which through endocrine, auto/paracrine action on VDR: 1) decreases the intensity of Cytokine and Chemokine storm, 2)modulating neutrophil activity, 3)maintaining the integrity of the pulmonary epithelial barrier, 4)stimulating epithelial repair and 5)decreasing directly and indirectly the risk of hypercoagulability and pulmonary or systemic thrombosis SARS-CoV-2: severe acute respiratory syndrome coronavirus 2. IFN-α, IFN-γ: Interferon gamma α and γ; IL-1β, IL-6, IL-12, IL-18, IL-33 (Interleukin -1β, 6, 12, 18, 33) TNF-α (Tumor Necrosis Factor-α). TGFβ (Transforming growth factor α and β). CCL2, CCL3, CCL5 Chemokine (C-C motif) ligand 2,3.5) CXCL8, CXCL9, CXCL10: C-X-C (motif chemokine ligand 8,910).
Fig. 2
Fig. 2
The Renin Angiotensin System (RAS) and Acute Respiratory Distress Syndrome (ARDS). Local or systemic inflammatory reactions may activate RAS and ACE thereby generating angiotensin II, which via its receptor (ATR) is able to induce lung damage. During SARS-CoV-2 invasion ACE2 is downregulated in Type II alveolar epithelial cells thereby decreasing the conversion of Ang II to Ang-(1–7). This prevents the protective action of the Ang (1–7), acting on its receptor (Mas R), and all aspects of ARDS. 1α,25(OH)2D/VDR is a powerful negative regulator of the renin-angiotensin system (RAS) inhibiting renin and the ACE/Ang II/AT1R cascade and inducing ACE2/Ang-(1–7) axis activity. ACII: cuboidal alveolar type II cells. SARS-CoV-2: severe acute respiratory syndrome coronavirus 2 Ang I angiotensin I. Ang II: angiotensin II. Ang-(1–7) angiotensin1–7. MasR: G protein-coupled Mas receptor. AT1R y AT2R: angiotensin II receptor 1 and 2.

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Source: PubMed

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