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Am J Physiol Lung Cell Mol Physiol (August 12, 2005). doi:10.1152/ajplung.00050.2005
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Submitted on January 26, 2005
Accepted on August 11, 2005

Involvement of the platelet activating factor receptor in host defense against Streptococcus pneumoniae during postinfluenza pneumonia

Koenraad F van der Sluijs1*, Leontine J. R. van Elden2, Monique Nijhuis2, Rob Schuurman2, Sandrine Florquin3, Takao Shimizu4, Satosh Ishii5, Henk M Jansen6, Rene Lutter7, and Tom van der Poll8

1 Laboratory of Experimental Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands; Department of Pulmonology, Academic Medical Center, Amsterdam, The Netherlands; Laboratory of Experimental Immunology, Academic Medical Center, Amsterdam, The Netherlands
2 Eijkman-Winkler Institute, Department of Virology, University Medical Center, Utrecht, The Netherlands
3 Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands
4 Department of Biochemistry and Molecular Biology, University of Tokyo, Tokyo, Japan
5 CREST of Japan Science and Technology Corporation, Tokyo, Japan
6 Department of Pulmonology, Academic Medical Center, Amsterdam, The Netherlands
7 Department of Pulmonology, Academic Medical Center, Amsterdam, The Netherlands; Laboratory of Experimental Immunology, Academic Medical Center, Amsterdam, The Netherlands
8 Laboratory of Experimental Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands

* To whom correspondence should be addressed. E-mail: kvandersluijs{at}amc.uva.nl.

Although influenza infection alone may lead to pneumonia, secondary bacterial infections are a much more common cause of pneumonia. Streptococcus (S.) pneumoniae is the most frequently isolated causative pathogen during postinfluenza pneumonia. Considering that S. pneumoniae utilizes the platelet-activating factor receptor (PAFR) to invade the respiratory epithelium and that the PAFR is upregulated during viral infection, we here used PAFR gene deficient (PAFR-/-) mice to determine the role of this receptor during postinfluenza pneumococcal pneumonia. Viral clearance was similar in wildtype and PAFR-/- mice and influenza virus was completely removed from the lungs at the time mice were inoculated with S. pneumoniae(day 14 after influenza infection). PAFR-/- mice displayed a significantly reduced bacterial outgrowth in their lungs, a diminished dissemination of the infection and a prolonged survival. Pulmonary levels of IL-10 and KC were significantly lower in PAFR-/- mice, whereas IL-6 and TNF-{alpha} were only trendwise lower. These data indicate that the pneumococcus uses the PAFR leading to severe pneumonia in a host previously exposed to influenza A.




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