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In order to consider effects of cellular mediators, the coagulation cascade must be inhibited to avoid clotting. There is considerable variation in the anticoagulants used among studies of<jats:italic>N<\/jats:italic>.<jats:italic>meningitidis<\/jats:italic>whole blood infections, featuring citrate, heparin or derivatives of hirudin, a polypeptide from leech saliva. Here, we compare the influence of these three different anticoagulants, and additionally Mg\/EGTA, on host innate immune responses as well as on viability of<jats:italic>N<\/jats:italic>.<jats:italic>meningitidis<\/jats:italic>strains isolated from healthy carriers and disease cases, reflecting different sequence types and capsule phenotypes. We found that the anticoagulants significantly impact on cellular responses and, strain-dependently, also on bacterial survival. Hirudin does not inhibit complement and is therefore superior over the other anticoagulants; indeed hirudin-plasma most closely reflects the characteristics of serum during<jats:italic>N<\/jats:italic>.<jats:italic>meningitidis<\/jats:italic>infection. We further demonstrate the impact of heparin on complement activation on<jats:italic>N<\/jats:italic>.<jats:italic>meningitidis<\/jats:italic>and its consequences on meningococcal survival in immune sera, which appears to be independent of the heparin binding antigens Opc and NHBA.<\/jats:p>","DOI":"10.1038\/s41598-018-28583-8","type":"journal-article","created":{"date-parts":[[2018,6,29]],"date-time":"2018-06-29T14:53:51Z","timestamp":1530284031000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Anticoagulants impact on innate immune responses and bacterial survival in whole blood models of Neisseria meningitidis infection"],"prefix":"10.1038","volume":"8","author":[{"given":"Lea","family":"Strobel","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9589-290X","authenticated-orcid":false,"given":"Kay O.","family":"Johswich","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2018,7,5]]},"reference":[{"key":"28583_CR1","doi-asserted-by":"publisher","first-page":"821","DOI":"10.1099\/jmm.0.45529-0","volume":"53","author":"SP Yazdankhah","year":"2004","unstructured":"Yazdankhah, S. P. & Caugant, D. A. Neisseria meningitidis: an overview of the carriage state. Journal of medical microbiology 53, 821\u2013832, https:\/\/doi.org\/10.1099\/jmm.0.45529-0 (2004).","journal-title":"Journal of medical microbiology"},{"key":"28583_CR2","doi-asserted-by":"crossref","unstructured":"van Deuren, M., Brandtzaeg, P. & van der Meer, J. W. Update on meningococcal disease with emphasis on pathogenesis and clinical management. Clinical microbiology reviews 13 144\u2013166, table of contents (2000).","DOI":"10.1128\/CMR.13.1.144"},{"key":"28583_CR3","doi-asserted-by":"publisher","first-page":"98","DOI":"10.4161\/viru.26515","volume":"5","author":"LA Lewis","year":"2014","unstructured":"Lewis, L. A. & Ram, S. Meningococcal disease and the complement system. 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