Journal
MICROBIOLOGY-SGM
Volume 161, Issue -, Pages 621-627Publisher
MICROBIOLOGY SOC
DOI: 10.1099/mic.0.000019
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Funding
- Alfred Osterlund Foundation
- Crafoord Foundation
- Greta and Johan Kock Foundation
- Knut and Alice Wallenberg Foundation
- Ragnar Soderberg Foundation
- Medical Faculty at Lund University
- Swedish Foundation for Strategic Research
- Swedish Research Council
- Swedish Society for Medical Research
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Recent work has shown that coagulation and innate immunity are tightly interwoven host responses that help eradicate an invading pathogen. Some bacterial species, including Staphylococcus aureus, secrete pro-coagulant factors that, in turn, can modulate these immune reactions. Such mechanisms may not only protect the micro-organism from a lethal attack, but also promote bacterial proliferation and the establishment of infection. Our data showed that coagulase-positive S. aureus bacteria promoted clotting of plasma which was not seen when a coagulase-deficient mutant strain was used. Furthermore, in vitro studies showed that this ability constituted a mechanism that supported the aggregation, survival and persistence of the microorganism within the fibrin network. These findings were also confirmed when agglutination and persistence of coagulase-positive S. aureus bacteria at the local focus of infection were studied in a subcutaneous murine infection model. In contrast, the coagulase-deficient S. aureus strain which was not able to induce clotting failed to aggregate and to persist in vivo. In conclusion, our data suggested that coagulase-positive S. aureus have evolved mechanisms that prevent their elimination within a fibrin clot.
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