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While the release of NETs is an attempt by neutrophils to trap pathogens and constrain infections, NETs can have bystander effects on the host by inducing uncontrolled thrombosis, inflammation, and tissue damage. From an evolutionary perspective, pathogens have adapted to bypass the host innate immune response.\n            <jats:italic>Staphylococcus aureus<\/jats:italic>\n            (\n            <jats:italic>S. aureus<\/jats:italic>\n            ), in particular, proficiently overcomes NET formation using several virulence factors. Here we review mechanisms of NET formation and how these are intertwined with platelet activation, the release of endothelial von Willebrand factor, and the activation of the coagulation system. We discuss the unique ability of\n            <jats:italic>S. aureus<\/jats:italic>\n            to modulate NET formation and alter released NETs, which helps\n            <jats:italic>S. aureus<\/jats:italic>\n            to escape from the host\u2019s defense mechanisms. We then discuss how platelets and the coagulation system could play a role in NET formation in\n            <jats:italic>S. aureus<\/jats:italic>\n            -induced infective endocarditis, and we explain how targeting these complex cellular interactions could reveal novel therapies to treat this disease and other immunothrombotic disorders.\n          <\/jats:p>","DOI":"10.1161\/atvbaha.121.316930","type":"journal-article","created":{"date-parts":[[2022,2,3]],"date-time":"2022-02-03T10:00:15Z","timestamp":1643882415000},"page":"261-276","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":53,"title":["<i>Staphylococcus aureus<\/i>\n            and Neutrophil Extracellular Traps: The Master Manipulator Meets Its Match in Immunothrombosis"],"prefix":"10.1161","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3481-4793","authenticated-orcid":true,"given":"Severien","family":"Meyers","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Belgium (S.M., M.C., P.V., K.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3164-512X","authenticated-orcid":true,"given":"Marilena","family":"Crescente","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Belgium (S.M., M.C., P.V., K.M.)."},{"name":"Department of Life Sciences, Manchester Metropolitan University, United Kingdom (M.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8698-2858","authenticated-orcid":true,"given":"Peter","family":"Verhamme","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Belgium (S.M., M.C., P.V., K.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1026-6107","authenticated-orcid":true,"given":"Kimberly","family":"Martinod","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Belgium (S.M., M.C., P.V., K.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1092385"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041050215"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00916048"},{"key":"e_1_3_2_5_2","first-page":"413","article-title":"XVI. 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