1887

Abstract

Recent work has shown that coagulation and innate immunity are tightly interwoven host responses that help eradicate an invading pathogen. Some bacterial species, including , 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 bacteria promoted clotting of plasma which was not seen when a coagulase-deficient mutant strain was used. Furthermore, studies showed that this ability constituted a mechanism that supported the aggregation, survival and persistence of the micro-organism within the fibrin network. These findings were also confirmed when agglutination and persistence of coagulase-positive bacteria at the local focus of infection were studied in a subcutaneous murine infection model. In contrast, the coagulase-deficient strain which was not able to induce clotting failed to aggregate and to persist . In conclusion, our data suggested that coagulase-positive have evolved mechanisms that prevent their elimination within a fibrin clot.

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2015-03-01
2022-01-19
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