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Journal of Virology, October 2004, p. 10303-10309, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10303-10309.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Signaling through the Prostaglandin I2 Receptor IP Protects against Respiratory Syncytial Virus-Induced Illness

Koichi Hashimoto,1,2 Barney S. Graham,3 Mark W. Geraci,4 Garret A. FitzGerald,5 Karine Egan,5 Weisong Zhou,1 Kasia Goleniewska,1 Jamye F. O'Neal,1 Jason D. Morrow,1 Russell K. Durbin,6 Peter F. Wright,7 Robert D. Collins,8 Tatsuo Suzutani,2 and R. Stokes Peebles Jr.1*

Department of Medicine,1 Department of Pediatrics,7 Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee,8 Department of Microbiology, Fukushima Medical University, Fukushima, Japan,2 Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland,3 Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado,4 Departments of Medicine and Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania,5 Department of Pediatrics, Ohio State University, Columbus, Ohio6

Received 18 November 2003/ Accepted 18 May 2004

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 PGI2 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.

* Corresponding author. Mailing address: Center for Lung Research, T-1217 MCN, Vanderbilt University Medical Center, Nashville, TN 37232-2650. Phone: (615) 322-3412. Fax: (615) 343-7448. E-mail: stokes.peebles{at}vanderbilt.edu.

Journal of Virology, October 2004, p. 10303-10309, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10303-10309.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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