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Antiviral Res. 2017 Jan;137:93-101. doi: 10.1016/j.antiviral.2016.11.004. Epub 2016 Nov 10.

Vitamin D increases the antiviral activity of bronchial epithelial cells in vitro.

Author information

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.

KEYWORDS:

Cathelicidin; Interferons; Respiratory viruses

PMID:
27838350
DOI:
10.1016/j.antiviral.2016.11.004
[Indexed for MEDLINE]
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