Staphylococcus aureus induces release of bradykinin in human plasma
(2001) In Infection and Immunity 69(6). p.3877-3882- Abstract
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.... (More)
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.
(Less)
- author
- Mattsson, E.
LU
; Herwald, H.
LU
; Cramer, H. ; Persson, K. LU ; Sjöbring, U. LU and Björck, L. LU
- organization
- publishing date
- 2001-06
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Infection and Immunity
- volume
- 69
- issue
- 6
- pages
- 3877 - 3882
- publisher
- American Society for Microbiology
- external identifiers
-
- pmid:11349054
- scopus:0035001194
- ISSN
- 0019-9567
- DOI
- 10.1128/IAI.69.6.3877-3882.2001
- language
- English
- LU publication?
- yes
- id
- 4ad26762-eed3-4576-aed2-1f48523c064e
- date added to LUP
- 2019-12-10 20:27:28
- date last changed
- 2023-01-08 06:06:05
@article{4ad26762-eed3-4576-aed2-1f48523c064e, abstract = {{<p>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.</p>}}, author = {{Mattsson, E. and Herwald, H. and Cramer, H. and Persson, K. and Sjöbring, U. and Björck, L.}}, issn = {{0019-9567}}, language = {{eng}}, number = {{6}}, pages = {{3877--3882}}, publisher = {{American Society for Microbiology}}, series = {{Infection and Immunity}}, title = {{Staphylococcus aureus induces release of bradykinin in human plasma}}, url = {{http://dx.doi.org/10.1128/IAI.69.6.3877-3882.2001}}, doi = {{10.1128/IAI.69.6.3877-3882.2001}}, volume = {{69}}, year = {{2001}}, }