Protective role of Indoleamine 2,3 dioxygenase in Respiratory Syncytial Virus associated immune response in airway epithelial cells.
RSV is a major cause of severe lower respiratory infection in infants and young children. With no vaccine yet available, it is important to clarify mechanisms of disease pathogenesis. Since indoleamine-2,3-dioxygenase (IDO) is an immunomodulatory enzyme and is upregulated with RSV infection, we studied it in vivo during infection of BALB/c mice and in vitro in A549 cells. RSV infection upregulated IDO transcripts in vivo and in vitro. IDO siRNA decreased IDO transcripts ~2 fold compared to control siRNA after RSV infection but this decrease did not affect RSV replication. In the presence of IFN-γ, siRNA-induced a decrease in IDO expression that was associated with an increase in virus replication and increased levels of IL-6, IL-8, CXCL10 and CCL4. Thus, our results show IDO is upregulated with RSV infection and this upregulation likely participates with IFN-γ in inhibition of virus replication and suppression of some host cell responses to infection.
['Rajan|Devi|D|', 'Chinnadurai|Raghavan|R|', "O'Keefe|Evan L|EL|", 'Boyoglu-Barnum|Seyhan|S|', 'Todd|Sean O|SO|', 'Hartert|Tina V|TV|', 'Galipeau|Jacques|J|', 'Anderson|Larry J|LJ|']
D000072283:A549 Cells D000818:Animals D016207:Cytokines D005260:Female D005786:Gene Expression Regulation D006801:Humans D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase D051379:Mice D008807:Mice, Inbred BALB C D034622:RNA Interference D012136:Respiratory Syncytial Viruses D015854:Up-Regulation D014779:Virus Replication
Respiratory Syncytial Virus IDO Chemokine Cytokine Tryptophan