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Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocard...
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Titel: |
Use of a Human-Like Low-Grade Bacteremia Model of Experimental Endocarditis To Study the Role of Staphylococcus aureus Adhesins and Platelet Aggregation in Early Endocarditis |
In: | Infection and Immunity, 81, 2013, 3, S. 697-703 |
veröffentlicht: |
American Society for Microbiology
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Umfang: | 697-703 |
ISSN: |
0019-9567 1098-5522 |
DOI: | 10.1128/iai.01030-12 |
Zusammenfassung: | <jats:title>ABSTRACT</jats:title><jats:p>Animal models of infective endocarditis (IE) induced by high-grade bacteremia revealed the pathogenic roles of<jats:named-content xmlns:xlink="http://www.w3.org/1999/xlink" content-type="genus-species" xlink:type="simple">Staphylococcus aureus</jats:named-content>surface adhesins and platelet aggregation in the infection process. In humans, however,<jats:named-content xmlns:xlink="http://www.w3.org/1999/xlink" content-type="genus-species" xlink:type="simple">S. aureus</jats:named-content>IE possibly occurs through repeated bouts of low-grade bacteremia from a colonized site or intravenous device. Here we used a rat model of IE induced by continuous low-grade bacteremia to explore further the contributions of<jats:named-content xmlns:xlink="http://www.w3.org/1999/xlink" content-type="genus-species" xlink:type="simple">S. aureus</jats:named-content>virulence factors to the initiation of IE. Rats with aortic vegetations were inoculated by continuous intravenous infusion (0.0017 ml/min over 10 h) with 10<jats:sup>6</jats:sup>CFU of<jats:italic>Lactococcus lactis</jats:italic>pIL253 or a recombinant<jats:italic>L. lactis</jats:italic>strain expressing an individual<jats:named-content xmlns:xlink="http://www.w3.org/1999/xlink" content-type="genus-species" xlink:type="simple">S. aureus</jats:named-content>surface protein (ClfA, FnbpA, BCD, or SdrE) conferring a particular adhesive or platelet aggregation property. Vegetation infection was assessed 24 h later. Plasma was collected at 0, 2, and 6 h postinoculation to quantify the expression of tumor necrosis factor (TNF), interleukin 1α (IL-1α), IL-1β, IL-6, and IL-10. The percentage of vegetation infection relative to that with strain pIL253 (11%) increased when binding to fibrinogen was conferred on<jats:italic>L. lactis</jats:italic>(ClfA strain) (52%;<jats:italic>P</jats:italic>= 0.007) and increased further with adhesion to fibronectin (FnbpA strain) (75%;<jats:italic>P</jats:italic>< 0.001). Expression of fibronectin binding alone was not sufficient to induce IE (BCD strain) (10% of infection). Platelet aggregation increased the risk of vegetation infection (SdrE strain) (30%). Conferring adhesion to fibrinogen and fibronectin favored IL-1β and IL-6 production. Our results, with a model of IE induced by low-grade bacteremia, resembling human disease, extend the essential role of fibrinogen binding in the initiation of<jats:named-content xmlns:xlink="http://www.w3.org/1999/xlink" content-type="genus-species" xlink:type="simple">S. aureus</jats:named-content>IE. Triggering of platelet aggregation or an inflammatory response may contribute to or promote the development of IE.</jats:p> |
Format: | E-Article |
Quelle: | American Society for Microbiology (CrossRef) |
Sprache: | Englisch |