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Does fibrinogen serve the host or the microbe in Staphylococcus infection?

Negrón, Oscar; Flick, Matthew J.

doi: 10.1097/MOH.0000000000000527
HEMOSTASIS AND THROMBOSIS: Edited by Alvin H. Schmaier

Purpose of review Fibrin(ogen) is a multifunctional clotting protein that not only has critical roles in hemostasis but is also important in inflammatory processes that control bacterial infection. As a provisional extracellular matrix protein, fibrin(ogen) functions as a physical barrier, a scaffold for immune cell migration, or as a spatially-defined cue to drive inflammatory cell activation. These mechanisms contribute to overall host antimicrobial defense against infection. However, numerous bacterial species have evolved mechanisms to manipulate host fibrin(ogen) to promote microbial virulence and survival. Staphylococcal species, in particular, express numerous virulence factors capable of engaging fibrin(ogen), promoting fibrin formation, and driving the dissolution of fibrin matrices.

Recent findings Recent studies have highlighted both new insights into the molecular mechanisms involved in fibrin(ogen)-mediated host defense and pathogen-driven virulence. Of particular interest is the role of fibrin(ogen) in forming host protective biofilms versus pathogen protective barriers and biofilms as well as the role of fibrin(ogen) in mediating direct host antimicrobial responses.

Summary Current data suggest that the role of fibrin(ogen) in staphylococcal infection is highly context-dependent and that better defining the precise cellular and molecular pathways activated will provide unique opportunities of therapeutic intervention to better treat Staphylococcal disease.

Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA

Correspondence to Matthew J. Flick, PhD, Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Mary Ellen Jones Building, 116 Manning Drive, Chapel Hill, North Carolina, 27599. Tel: +1 919 843 1339; e-mail:

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