Open AccessStaphylococcus aureus Induces Release of Bradykinin in Human Plasma
Author(s) -
Eva Mattsson,
Heiko Herwald,
Henning Cramer,
Kristin A. Persson,
Ulf Sjöbring,
Lars Björck
Publication year - 2001
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.69.6.3877-3882.2001
Subject(s) - bradykinin , staphylococcus aureus , prekallikrein , microbiology and biotechnology , kininogen , biology , kallikrein , proinflammatory cytokine , streptococcus pyogenes , immunology , inflammation , bacteria , biochemistry , enzyme , receptor , genetics
Staphylococcus aureus is a prominent human pathogen. Here we report that intact S. aureus bacteria activate the contact system in human plasma in vitro, resulting in a massive release of the potent proinflammatory and vasoactive peptide bradykinin. In contrast, no such effect was recorded with Streptococcus pneumoniae. In the activation of the contact system, blood coagulation factor XII and plasma kallikrein play central roles, and a specific inhibitor of these serine proteinases inhibited the release of bradykinin by S. aureus in human plasma. Furthermore, fragments of the cofactor H-kininogen of the contact system efficiently blocked bradykinin release. The results suggest that activation of the contact system at the surface of S. aureus and the subsequent release of bradykinin could contribute to the hypovolemic hypotension seen in patients with severe S. aureus sepsis. The data also suggest that the contact system could be used as a target in the treatment of S. aureus infections.