@article{mbs:/content/journal/micro/10.1099/mic.0.000019, author = "Loof, Torsten G. and Goldmann, Oliver and Naudin, Clément and Mörgelin, Matthias and Neumann, Yvonne and Pils, Marina C. and Foster, Simon J. and Medina, Eva and Herwald, Heiko", title = "Staphylococcus aureus-induced clotting of plasma is an immune evasion mechanism for persistence within the fibrin network", journal= "Microbiology", year = "2015", volume = "161", number = "3", pages = "621-627", doi = "https://doi.org/10.1099/mic.0.000019", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.000019", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", 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 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 micro-organism 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.", }