title: Staphylococcus aureus-induced clotting of plasma is an immune evasion mechanism for persistence within the fibrin network.
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.
authors.affiliation: 1Department of Clinical Sciences, Division of Infection Medicine, Lund University, Lund, Sweden.|2Infection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
authors.forename: Torsten G
authors.initials: TG
authors.lastname: Loof
authors.affiliation: 2Infection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
authors.forename: Oliver
authors.initials: O
authors.lastname: Goldmann
authors.affiliation: 1Department of Clinical Sciences, Division of Infection Medicine, Lund University, Lund, Sweden.
authors.forename: Clément
authors.initials: C
authors.lastname: Naudin
authors.affiliation: 1Department of Clinical Sciences, Division of Infection Medicine, Lund University, Lund, Sweden.
authors.forename: Matthias
authors.initials: M
authors.lastname: Mörgelin
authors.affiliation: 3Institute of Molecular and Clinical Immunology, Otto-von-Guericke-University Magdeburg, Germany.|4Systems-oriented Immunology and Inflammation Research Group, Department of Immune Control, Helmholtz Centre for Infection Research, Braunschweig, Germany.
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Neumann
authors.affiliation: 5Mousepathology, Animal Experimental Unit, Helmholtz Centre for Infection Research, Braunschweig, Germany.
authors.forename: Marina C
authors.initials: MC
authors.lastname: Pils
authors.affiliation: 6Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, UK.
authors.forename: Simon J
authors.initials: SJ
authors.lastname: Foster
authors.affiliation: 2Infection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
authors.forename: Eva
authors.initials: E
authors.lastname: Medina
authors.affiliation: 1Department of Clinical Sciences, Division of Infection Medicine, Lund University, Lund, Sweden.
authors.forename: Heiko
authors.initials: H
authors.lastname: Herwald
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D001777:Blood Coagulation; D003030:Coagulase / Q000235:genetics / Q000378:metabolism; D005337:Fibrin / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D057131:Immune Evasion; D051379:Mice; D008808:Mice, Inbred CBA; D050296:Microbial Viability; D013203:Staphylococcal Infections / Q000097:blood* / Q000276:immunology / Q000382:microbiology; D013211:Staphylococcus aureus / Q000201:enzymology / Q000235:genetics / Q000254:growth & development / Q000276:immunology*
chemical_list: D001426:Bacterial Proteins; D003030:Coagulase; D005337:Fibrin