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    Institut für Hygiene und Mikrobiologie

    Paper from IHM research group in Scientific Reports: Influence of anticoagulants on whole blood models of Neisseria meningitidis infection.

    17.07.2018

    (Strobel and Johswich, Sci Rep. 2018 Jul 5;8(1):10225. doi: 10.1038/s41598-018-28583-8; https://www.nature.com/articles/s41598-018-28583-8)

    Modeling invasive meningococcal disease by ex vivo infection of human whole blood is a valuable tool to study host-pathogen interactions. This is particularly important for investigation of the human-restricted pathogen N. meningitidis, as it can cause blood stream infections and tightly interacts with the complement system and cells of the innate immune system.

    In order to conduct interpretable whole blood assays, coagulation must be inhibited. There are several anticoagulants available, including EDTA, citrate, heparin, or hirudin from leech saliva. However, the anticoagulants can significantly influence the outcomes of experimental ex vivo infection with meningococci, as Strobel et al. demonstrate: EDTA (and a similar component, EGTA) inhibit growth of all tested meningococcal strains in liquid growth media through sequestration of Mg2+ and /or Ca2+, and citrate inhibits growth of some of the tested strains. EDTA entirely blocks complement activation, the single most innate immue determinant protecting against invasive meningococcal disease. Heparin as well demonstrated significant impact on complement activation and deposition onto N. meningitidis. Only hirudin appeared to be a suitable anticoagulant for whole blood infections, as it did not interfere with complement or bacterial growth.

    Noteworthy, the study pointed out that heparin does not need to associate with the bacterial surface in order to protect N. meningitidis against complement-mediated lysis, although bacteria possess proteins such as the Neisseria heparin binding antigen (NHBA) or Opc, which reportedly bind to endogenous heparin.

     

    (Strobel and Johswich, Sci Rep. 2018 Jul 5;8(1):10225. doi: 10.1038/s41598-018-28583-8; www.nature.com/articles/s41598-018-28583-8

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