Signaling through the prostaglandin I2 receptor IP protects against respiratory syncytial virus-induced illness

Koichi Hashimoto, Barney S. Graham, Mark W. Geraci, Garret A. FitzGerald, Karine Egan, Weisong Zhou, Kasia Goleniewska, Jamye F. O'Neal, Jason D. Morrow, Russell K. Durbin, Peter F. Wright, Robert D. Collins, Tatsuo Suzutani, R. Stokes Peebles

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


The role of prostanoids in modulating respiratory syncytial virus (RSV) infection is unknown. We found that RSV infection in mice increases production of prostaglandin I2 (PGI2). Mice that overexpress PGI 2 synthase selectively in bronchial epithelium are protected against RSV-induced weight loss and have decreased peak viral replication and gamma interferon levels in the lung compared to nontransgenic littermates. In contrast, mice deficient in the PGI2 receptor IP have exacerbated RSV-induced weight loss with delayed viral clearance and increased levels of gamma interferon in the lung compared to wild-type mice. These results suggest that signaling through IP has antiviral effects while protecting against RSV-induced illness and that PGI2 is a potential therapeutic target in the treatment of RSV.

Original languageEnglish (US)
Pages (from-to)10303-10309
Number of pages7
JournalJournal of virology
Issue number19
StatePublished - Oct 2004

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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