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Here, we tested the hypothesis that direct binding between fibrin(ogen) and <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> is a component of the primary host antimicrobial response mechanism and prevention of secondary microbe dissemination from the peritoneal cavity. To establish a model system, we showed that fibrinogen isolated from Fib\u03b3<jats:sup>\u03945<\/jats:sup> mice, which express a mutant form lacking the final 5 amino acids of the fibrinogen \u03b3 chain (termed fibrinogen\u03b3<jats:sup>\u03945<\/jats:sup>), did not support <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> adherence when immobilized and clumping when in suspension. In contrast, purified wildtype fibrinogen supported robust adhesion and clumping that was largely dependent on <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> expression of the receptor clumping factor A (ClfA). Following peritoneal infection with <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> USA300, Fib\u03b3<jats:sup>\u03945<\/jats:sup> mice displayed worse survival compared to WT mice coupled to reduced bacterial killing within the peritoneal cavity and increased dissemination of the microbes into circulation and distant organs. The failure of acute bacterial killing, but not enhanced dissemination, was partially recapitulated by mice infected with <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> USA300 lacking ClfA. Fibrin polymer formation and coagulation transglutaminase Factor XIII each contributed to killing of the microbes within the peritoneal cavity, but only elimination of polymer formation enhanced systemic dissemination. Host macrophage depletion or selective elimination of the fibrin(ogen) \u03b22-integrin binding motif both compromised local bacterial killing and enhanced <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> systemic dissemination, suggesting fibrin polymer formation in and of itself was not sufficient to retain <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> within the peritoneal cavity. Collectively, these findings suggest that following peritoneal infection, the binding of <jats:italic>S<\/jats:italic>. <jats:italic>aureus<\/jats:italic> to stabilized fibrin matrices promotes a local, macrophage-mediated antimicrobial response essential for prevention of microbe dissemination and downstream host mortality.<\/jats:p>","DOI":"10.1371\/journal.ppat.1010227","type":"journal-article","created":{"date-parts":[[2022,1,18]],"date-time":"2022-01-18T20:08:00Z","timestamp":1642536480000},"page":"e1010227","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":22,"title":["Fibrin(ogen) engagement of S. aureus promotes the host antimicrobial response and suppression of microbe dissemination following peritoneal 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