Osong Public Health Res Perspect.  2018 Dec;9(6):334-339. 10.24171/j.phrp.2018.9.6.07.

Anti-Human Rhinovirus 1B Activity of Dexamethasone viaGCR-Dependent Autophagy Activation

• Lee JS
• Kim SR
• Song JH
• Lee YP
• Ko HJ

• KMID: 2431676
• DOI: http://doi.org/10.24171/j.phrp.2018.9.6.07

Abstract

OBJECTIVES
Human rhinoviruses (HRVs) are the major cause of the common cold. Currently there is no registered, clinically effective, antiviral chemotherapeutic agent to treat diseases caused by HRVs. In this study, the antiviral activity of dexamethasone (DEX) against HRV1B was examined.
METHODS
The anti-HRV1B activity of DEX was assessed by sulforhodamine B assay in HeLa cells, and by RT-PCR in the lungs of HRV1B-infected mice. Histological evaluation of HRV1B-infected lungs was performed and a histological score was given. Anti-HRV1B activity of DEX via the glucocorticoid receptor (GCR)-dependent autophagy activation was assessed by blocking with chloroquine diphosphate salt or bafilomycin A1 treatment.
RESULTS
In HRV1B-infected HeLa cells, treatment with DEX in a dose-dependent manner, resulted in a cell viability of > 70% indicating that HRV1B viral replication was reduced by DEX treatment. HRV1B infected mice treated with DEX, had evidence of reduced inflammation and a moderate histological score. DEX treatment showed antiviral activity against HRV1B via GCR-dependent autophagy activation.
CONCLUSION
This study demonstrated that DEX treatment showed anti-HRV1B activity via GCR-dependent autophagy activation in HeLa cells and HRV1B infected mice. Further investigation assessing the development of topical formulations may enable the development of improved DEX effectiveness.

Keyword

autophagy; dexamethasone; glucocorticoid receptor; rhinovirus

MeSH Terms

Animals
Autophagy*
Cell Survival
Chloroquine
Common Cold
Dexamethasone*
HeLa Cells
Humans
Inflammation
Lung
Mice
Receptors, Glucocorticoid
Rhinovirus*
Chloroquine
Dexamethasone
Receptors, Glucocorticoid