Aurica G Telcian1, Mihnea T Zdrenghea2, Michael R Edwards1, Vasile Laza-Stanca1, Patrick Mallia3, Sebastian L Johnston3, Luminita A Stanciu4. 1. Airways Disease Infection Section, National Heart and Lung Institute, Imperial College London, Medical Research Council, Asthma UK Centre in Allergic Mechanisms of Asthma, Centre for Respiratory Infections, London, UK. 2. Department of Hematology, Iuliu Hatieganu University of Medicine and Pharmacy Cluj-Napoca and Ion Chiricuta Oncology Institute, Cluj-Napoca, Romania. Electronic address: mzdrenghea@umfcluj.ro. 3. Airways Disease Infection Section, National Heart and Lung Institute, Imperial College London, Medical Research Council, Asthma UK Centre in Allergic Mechanisms of Asthma, Centre for Respiratory Infections, London, UK; Imperial College Healthcare NHS Trust, London, UK. 4. Airways Disease Infection Section, National Heart and Lung Institute, Imperial College London, Medical Research Council, Asthma UK Centre in Allergic Mechanisms of Asthma, Centre for Respiratory Infections, London, UK; Department of Hematology, Iuliu Hatieganu University of Medicine and Pharmacy Cluj-Napoca and Ion Chiricuta Oncology Institute, Cluj-Napoca, Romania.
Abstract
BACKGROUND: By modulating the antiviral immune response via vitamin D receptor, the active form of vitamin D (1,25-dihydroxyvitamin D, calcitriol) could play a central role in protection against respiratory virus infections. This in vitro study tested the hypothesis that respiratory viruses modulate vitamin D receptor expression in human bronchial epithelial cells and this modulation affects the antiviral response to exogenous vitamin D. METHODS: Human primary bronchial epithelial cells were infected with rhinoviruses and respiratory syncytial virus in the presence or absence of vitamin D. Expression of vitamin D receptor, 1α-hydroxylase (1α(OH)ase), 24-hydroxylase (24(OH)ase), innate interferons, interferon stimulated genes and cathelicidin were measured by quantitative polymerase chain reaction. The antiviral effect of vitamin D on rhinovirus replication was determined by measurement of virus load. A direct inactivation assay was used to determine the antiviral activity of cathelicidin. RESULTS: Both RV and RSV decreased vitamin D receptor and 24(OH)ase and, in addition, RSV increased 1α(OH)ase expression in epithelial cells. Vitamin D decreased rhinovirus replication and release, and increased rhinovirus-induced interferon stimulated genes and cathelicidin. Furthermore, cathelicidin had direct anti-rhinovirus activity. CONCLUSIONS: Despite lower vitamin D receptor levels in rhinovirus-infected epithelial cells, exogenous vitamin D increased antiviral defences most likely via cathelicidin and innate interferon pathways.
BACKGROUND: By modulating the antiviral immune response via vitamin D receptor, the active form of vitamin D (1,25-dihydroxyvitamin D, calcitriol) could play a central role in protection against respiratory virus infections. This in vitro study tested the hypothesis that respiratory viruses modulate vitamin D receptor expression in human bronchial epithelial cells and this modulation affects the antiviral response to exogenous vitamin D. METHODS: Human primary bronchial epithelial cells were infected with rhinoviruses and respiratory syncytial virus in the presence or absence of vitamin D. Expression of vitamin D receptor, 1α-hydroxylase (1α(OH)ase), 24-hydroxylase (24(OH)ase), innate interferons, interferon stimulated genes and cathelicidin were measured by quantitative polymerase chain reaction. The antiviral effect of vitamin D on rhinovirus replication was determined by measurement of virus load. A direct inactivation assay was used to determine the antiviral activity of cathelicidin. RESULTS: Both RV and RSV decreased vitamin D receptor and 24(OH)ase and, in addition, RSV increased 1α(OH)ase expression in epithelial cells. Vitamin D decreased rhinovirus replication and release, and increased rhinovirus-induced interferon stimulated genes and cathelicidin. Furthermore, cathelicidin had direct anti-rhinovirus activity. CONCLUSIONS: Despite lower vitamin D receptor levels in rhinovirus-infected epithelial cells, exogenous vitamin D increased antiviral defences most likely via cathelicidin and innate interferon pathways.
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