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Protective role of Indoleamine 2,3 dioxygenase in Respiratory Syncytial Virus associated immune response in airway epithelial cells.

Authors
  • Rajan, Devi1
  • Chinnadurai, Raghavan2
  • Keefe, Evan O1
  • Boyoglu-Barnum, Seyhan3
  • Todd, Sean O1
  • Hartert, Tina V4
  • Galipeau, Jacques2
  • Anderson, Larry J5
  • 1 Department of Pediatrics, Emory Children's Center, Emory University and Children's Healthcare of Atlanta, Atlanta, Georgia. , (Georgia)
  • 2 Department of Medicine, University of Wisconsin Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI, USA.
  • 3 VPL, VRC, NIAID, NIH, DHHS, Bethesda, MD, USA.
  • 4 Department of Medicine, Vanderbilt Institute for Medicine & Public Health, Nashville, TN, USA.
  • 5 Department of Pediatrics, Emory Children's Center, Emory University and Children's Healthcare of Atlanta, Atlanta, Georgia. Electronic address: [email protected] , (Georgia)
Type
Published Article
Journal
Virology
Publisher
Elsevier
Publication Date
Dec 01, 2017
Volume
512
Pages
144–150
Identifiers
DOI: 10.1016/j.virol.2017.09.007
PMID: 28963880
Source
Medline
Keywords
License
Unknown

Abstract

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.

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