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Streptococcus pneumoniae is the most common causative pathogen in community-acquired pneumonia. Protease-activated receptor 2 (PAR2) is expressed by different cell types in the lungs and can mediate inflammatory responses. We sought to determine the role of PAR2 during pneumococcal pneumonia. Pneumococcal pneumonia or sepsis was induced in wild-type and PAR2 knock-out (Par2-/-) mice by infection with viable S. pneumoniae. Par2-/- mice demonstrated improved host defense, a largely preserved lung barrier integrity, and reduced mortality during pneumococcal pneumonia. PAR2 deficiency did not influence bacterial growth after intravenous infection. Inhibition of the endogenous PAR2 activating proteases tissue factor/factor VIIa or tryptase did not impact on bacterial burdens during pneumonia. In a PAR2 reporter cell line it was demonstrated that S. pneumoniae-derived proteases are able to cleave PAR2. These results show that S. pneumoniae is able to cleave and exploit PAR2 to disseminate systemically from the airways.

Original publication




Conference paper

Publication Date





1462 - 1471


Center for Experimental and Molecular Medicine (CEMM), The Netherlands.


Animals, Mice, Inbred C57BL, Mice, Knockout, Humans, Mice, Streptococcus pneumoniae, Pneumonia, Pneumococcal, Inflammation, Helminth Proteins, Receptor, PAR-2, Specific Pathogen-Free Organisms, Gene Expression Regulation, Blood Coagulation, HEK293 Cells, Bacterial Load