| Autor: |
Braff MH; Division of Infectious Disease, Children's Hospital and Regional Medical Center, University of Washington, Seattle, WA 98109, USA., Jones AL, Skerrett SJ, Rubens CE |
| Jazyk: |
angličtina |
| Zdroj: |
The Journal of infectious diseases [J Infect Dis] 2007 May 01; Vol. 195 (9), pp. 1365-72. Date of Electronic Publication: 2007 Mar 15. |
| DOI: |
10.1086/513277 |
| Abstrakt: |
The increasing prevalence of Staphylococcus aureus strains isolated from hospital- and community-acquired respiratory tract infections is an important public health concern worldwide. The majority of S. aureus strains produce staphylokinase, a plasminogen activator capable of inactivating neutrophil alpha-defensins and of impairing phagocytosis via opsonin degradation. Cathelicidin antimicrobial peptides are present at sites of infection before the release of neutrophil alpha-defensins. Therefore, we hypothesized that staphylokinase interacts with cathelicidin during the early pathogenesis of S. aureus airway infection. In a mouse intranasal infection model, cathelicidin was strongly up-regulated in the airways during the development of staphylococcal pneumonia. In vitro, cathelicidin bound directly to staphylokinase and augmented staphylokinase-dependent plasminogen activation and fibrinolysis at concentrations consistent with those detected in the airways during infection. These data suggest that staphylokinase production may be a novel virulence mechanism by which S. aureus exploits cathelicidin to promote fibrinolysis, leading to enhanced bacterial dissemination and invasive infection. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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