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

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

Submitted 26 January 2005 ; accepted in final form 11 August 2005

Although influenza infection alone may lead to pneumonia, secondary bacterial infections are a much more common cause of pneumonia. Streptococcus 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 wild-type 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- 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.

virus; bacteria; pneumonia; inflammation

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