1. Vitamin D attenuates rhinovirus-induced expression of intercellular adhesion molecule-1 (ICAM-1) and platelet-activating factor receptor (PAFR) in respiratory epithelial cells.
- Author
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Greiller CL, Suri R, Jolliffe DA, Kebadze T, Hirsman AG, Griffiths CJ, Johnston SL, and Martineau AR
- Subjects
- A549 Cells, Calcitriol pharmacology, Epithelial Cells drug effects, Epithelial Cells metabolism, Epithelial Cells virology, Host-Parasite Interactions drug effects, Humans, Picornaviridae Infections genetics, Respiratory Mucosa drug effects, Respiratory Mucosa metabolism, Respiratory Mucosa virology, Rhinovirus physiology, Vitamin D pharmacology, Gene Expression Regulation drug effects, Intercellular Adhesion Molecule-1 genetics, Picornaviridae Infections prevention & control, Platelet Membrane Glycoproteins genetics, Receptors, G-Protein-Coupled genetics, Rhinovirus drug effects, Vitamin D analogs & derivatives, Vitamins pharmacology
- Abstract
Human rhinoviruses commonly cause upper respiratory infections, which may be complicated by secondary bacterial infection. Vitamin D replacement reduces risk of acute respiratory infections in vitamin D-deficient individuals, but the mechanisms by which such protection is mediated are incompletely understood. We therefore conducted experiments to characterise the influence of the major circulating metabolite 25-hydroxyvitamin D (25[OH]D) and the active metabolite 1,25-dihydroxyvitamin D (1,25[OH]
2 D) on responses of a respiratory epithelial cell line (A549 cells) to infection with a major group human rhinovirus (RV-16). Pre-treatment of A549 respiratory epithelial cells with a physiological concentration (10-7 M) of 25(OH)D induced transient resistance to infection with RV-16 and attenuated RV-16-induced expression of the genes encoding intercellular adhesion molecule 1 (ICAM-1, a cell surface glycoprotein that acts as the cellular receptor for major group rhinoviruses) and platelet-activating factor receptor (PAFR, a G-protein coupled receptor implicated in adhesion of Streptococcus pneumoniae to respiratory epithelial cells). These effects were associated with enhanced expression of the genes encoding the NF-κB inhibitor IκBα and the antimicrobial peptide cathelicidin LL-37. Our findings suggest possible mechanisms by which vitamin D may enhance resistance to rhinovirus infection and reduce risk of secondary bacterial infection in vitamin D-deficient individuals., (Crown Copyright © 2018. Published by Elsevier Ltd. All rights reserved.)- Published
- 2019
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