{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T19:10:59Z","timestamp":1790363459882,"version":"4.1.0"},"reference-count":67,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,6,25]],"date-time":"2013-06-25T00:00:00Z","timestamp":1372118400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2013,8]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:italic><jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>eisseria meningitidis<\/jats:italic> (<jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m) is a leading cause of septicemia in childhood. <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m septicemia is unique with respect to very quick disease progression, high <jats:italic>in vivo<\/jats:italic> bacterial replication rate and its considerable mortality. <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m circumvents major mechanisms of innate immunity such as complement system and phagocytosis. Neutrophil extracellular traps (<jats:styled-content style=\"fixed-case\">NETs<\/jats:styled-content>) are formed from neutrophils during systemic infection and are suggested to contain invading microorganisms. Here, we investigated the interaction of <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m with <jats:styled-content style=\"fixed-case\">NETs<\/jats:styled-content>. Both, meningococci and spontaneously released outer membrane vesicles (<jats:styled-content style=\"fixed-case\">SOMVs<\/jats:styled-content>) were potent <jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content> inducers. <jats:styled-content style=\"fixed-case\">NETs<\/jats:styled-content> were unable to kill <jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content> bound meningococci, but slowed down their proliferation rate. Using <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m as model organism we identified three novel mechanisms how bacteria can evade <jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content>\u2010mediated killing: (i) modification of lipid <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> of meningococcal <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> with phosphoethanolamine protected <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m from <jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content>\u2010bound cathepsin <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>; (ii) expression of the high\u2010affinity zinc uptake receptor <jats:styled-content style=\"fixed-case\">ZnuD<\/jats:styled-content> allowed <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m to escape <jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content>\u2010mediated nutritional immunity; (iii) binding of <jats:styled-content style=\"fixed-case\">SOMVs<\/jats:styled-content> to <jats:styled-content style=\"fixed-case\">NETs<\/jats:styled-content> saved <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m from <jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content> binding and the consequent bacteriostatic effect. Escape from <jats:styled-content style=\"fixed-case\">NETs<\/jats:styled-content> may contribute to the most rapid progression of meningococcal disease. The induction of <jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content> formation by <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>m <jats:italic>in vivo<\/jats:italic> might aggravate thrombosis in vessels ultimately directing to disseminated intravascular coagulation (<jats:styled-content style=\"fixed-case\">DIC<\/jats:styled-content>).<\/jats:p>","DOI":"10.1111\/mmi.12288","type":"journal-article","created":{"date-parts":[[2013,6,10]],"date-time":"2013-06-10T08:21:27Z","timestamp":1370852487000},"page":"433-449","source":"Crossref","is-referenced-by-count":90,"title":["<i>In vitro<\/i> resistance mechanisms of <i><scp>N<\/scp>eisseria meningitidis<\/i> against neutrophil extracellular traps"],"prefix":"10.1111","volume":"89","author":[{"given":"Martin","family":"Lappann","sequence":"first","affiliation":[{"name":"Institute for Hygiene and Microbiology University of Wuerzburg  Wuerzburg 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