IFN-a production by human mononuclear cells infected with varicella-zoster virus through TLR9-dependent and-independent pathways

Understanding the defense mechanisms of the host of an organism is important for infection control.In previous studies,we demonstrated that interferon-a(IFN-a),but not IL-12,was produced by human peripheral blood mononuclear cells infected with varicella-zoster virus(VZV).Here,we investigated what kind of cell(s)and which signal molecule(s)are involved in IFN-a production.Using cell isolation and ELISA,we found that plasmacytoid dendritic cells(pDCs)were responsible for IFN-a production during VZV infection.We also found that Toll-like receptor 9(TLR9)was involved in VZV-induced IFN-a production because inhibitory CpG oligodeoxynucleotide inhibited IFN-a production.UV-inactivated VZV-induced IFN-a production was lower than that of active VZV,indicating another TLR9-independent pathway.Further studies demonstrated that double-stranded RNA-dependent protein kinase,but not DNA-dependent protein kinase was involved in VZV-induced IFN-a production.Together,these results suggest that pDCs play an important role in IFN-a production during VZV infection through TLR9-dependent and-independent pathways.

Prenatal glucocorticoid contributed to rat lung dysplasia is related to asymmetric dimethylarginine/nitric oxide pathway

Prenatal glucocorticoids(GCs) have been used to induce maturation of preterm fetal lungs and prevent the development of respiratory distress syndrome of the premature. Pulmonary surfactant induction has been regarded as the most important effect of prenatal GCs. However,report about the prolonged effects of prenatal GCs on the development of rat lung is of limited. In this study, we tried to investigate the acute and chronic modulation effects of prenatal dexamethasone(DEX) to asymmetric dimethylarginine(ADMA)/nitric oxide(NO) signal pathway of lung tissue. Pregnant Sprague Dawley rats at gestational day 14–20 were administered i.p. DEX(0.1 mg kg-1d-1).Acute programming effects of prenatal DEX were assessed at postnatal day 7, and long-term programming effects of offspring were assessed at day 120. We found that repetitive prenatal DEX exposure contributes to DNA oxidative damage and alveolar tissue dysplasia. Prenatal DEXtreatment decreased ADMA and increased i NOS expression. Prenatal DEX treatment also increased TNF-a transcript expression and decreased HDAC2 protein expression at acute stage. In conclusion, repetitive prenatal DEX has prolonged stress damage effects on lung tissue.