The Journal of Experimental Medicine
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Published 16 May 2005. doi:10.1084/jem.20042041
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 10, 1669-1676
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ARTICLE

 Induction of vascular leakage through release of bradykinin and a novel kinin by cysteine proteinases from Staphylococcus aureus

Takahisa Imamura1, Sumio Tanase2, Grzegorz Szmyd3, Andrzej Kozik4, James Travis5, and Jan Potempa3,5

1 Division of Molecular Pathology, Graduate School of Medical and Pharmaceutical Sciences
2 Department of Analytical Biochemistry, School of Health Sciences, Kumamoto University, Kumamoto 860-8556, Japan
3 Department of Microbiology, Faculty of Biotechnology, Jagiellonian University, 31-007 Kraków, Poland
4 Department of Analytical Biochemistry, Faculty of Biotechnology, Jagiellonian University, 31-007 Kraków, Poland
5 Department of Biochemistry and Molecular Biology, University of Georgia, Athens, GA 30602

CORRESPONDENCE Takahisa Imamura: taka{at}kaiju.medic.kumamoto-u.ac.jp

Staphylococcus aureus is a major pathogen of gram-positive septic shock and frequently is associated with consumption of plasma kininogen. We examined the vascular leakage (VL) activity of two cysteine proteinases that are secreted by S. aureus. Proteolytically active staphopain A (ScpA) induced VL in a bradykinin (BK) B2-receptor–dependent manner in guinea pig skin. This effect was augmented by staphopain B (SspB), which, by itself, had no VL activity. ScpA also produced VL activity from human plasma, apparently by acting directly on kininogens to release BK, which again was augmented significantly by SspB. Intravenous injection of ScpA into a guinea pig caused BK B2-receptor–dependent hypotension. ScpA and SspB together induced the release of leucyl-methionyl-lysyl-BK, a novel kinin with VL and blood pressure–lowering activities that are equivalent to BK. Collectively, these data suggest that production of BK and leucyl-methionyl-lysyl-BK by staphopains is a new mechanism of S. aureus virulence and bacterial shock. Therefore, staphopain-specific inhibitors and kinin-receptor antagonists could be used to treat this disease.

Abbreviations used: BK, bradykinin; BP, blood pressure; HK, high molecular weight kininogen; LK, low molecular weight kininogen; SBTI, soybean trypsin inhibitor; ScpA, staphopain A; SspB, staphopain B; TBS, Tris-buffered saline; VL, vascular leakage.


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