Abstract
Ginseng has been used in humans for thousands of years but its effects on viral infection have not been well understood. We investigated the effects of red ginseng extract (RGE) on respiratory syncytial virus (RSV) infection using in vitro cell culture and in vivo mouse models. RGE partially protected human epithelial (HEp2) cells from RSV-induced cell death and viral replication. In addition, RGE significantly inhibited the production of RSV-induced pro-inflammatory cytokine (TNF-α) in murine dendritic and macrophage-like cells. More importantly, RGE intranasal pre-treatment prevented loss of mouse body weight after RSV infection. RGE treatment improved lung viral clearance and enhanced the production of interferon (IFN-γ) in bronchoalveolar lavage cells upon RSV infection of mice. Analysis of cellular phenotypes in bronchoalveolar lavage fluids showed that RGE treatment increased the populations of CD8+ T cells and CD11c+ dendritic cells upon RSV infection of mice. Taken together, these results provide evidence that ginseng has protective effects against RSV infection through multiple mechanisms, which include improving cell survival, partial inhibition of viral replication and modulation of cytokine production and types of immune cells migrating into the lung.
Highlights
Respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, is a negative single-stranded RNA virus
We investigated the potential effects of red ginseng extract (RGE) on respiratory syncytial virus (RSV)-induced cytopathogenic formation and viral replication in human epithelial cells
Since epithelial cells are the primary targets of RSV infection [28], we investigated the possible effects of RGE on RSV infection in human epithelial (HEp2) cells
Summary
Respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, is a negative single-stranded RNA virus. RSV is the leading cause of serious respiratory disease in infants and immune-suppressed populations [1,2]. It was reported that high levels of proinflammatory cytokines including IL-4, IL-5 and IL-6 were associated with acute bronchiolitis in RSV-infected children [3]. These data were consistent with excessive T helper type 2 and/or deficient type 1 immune responses in RSV bronchiolitis [1,9]. Dendritic cells are uniquely positioned to link innate to adaptive immune responses and may play a role in modulating bronchiolitis [11]
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