Complement Activation Induced by PurifiedNeisseria meningitidisLipopolysaccharide (LPS), Outer Membrane Vesicles, Whole Bacteria, and an LPS‐Free Mutant | Zendy

Anna Bjerre | Zendy; Berit Brusletto | Zendy; Tom Eirik Mollnes | Zendy; Elisabeth Fritzsønn | Zendy; Einar Rosenqvist | Zendy; Elisabeth Wedege | Zendy; Ellen Namork | Zendy; Peter Kierulf | Zendy; P Brandtzæg | Zendy

Open Access

Complement Activation Induced by PurifiedNeisseria meningitidisLipopolysaccharide (LPS), Outer Membrane Vesicles, Whole Bacteria, and an LPS‐Free Mutant

Author(s) -

Anna Bjerre,

Berit Brusletto,

Tom Eirik Mollnes,

Elisabeth Fritzsønn,

Einar Rosenqvist,

Elisabeth Wedege,

Ellen Namork,

Peter Kierulf,

P Brandtzæg

Publication year - 2002

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/338269

Subject(s) - neisseria meningitidis , bacterial outer membrane , lipopolysaccharide , complement system , complement membrane attack complex , microbiology and biotechnology , alternative complement pathway , classical complement pathway , vesicle , chemistry , bacteria , mutant , biology , antibody , biochemistry , membrane , escherichia coli , immunology , genetics , gene

Complement activation is closely associated with plasma endotoxin levels in patients with meningococcal infections. This study assessed complement activation induced by purified Neisseria meningitidis lipopolysaccharide (Nm-LPS), native outer membrane vesicles (nOMVs), LPS-depleted outer membrane vesicles (dOMVs), wild-type meningococci, and an LPS-free mutant (lpxA(-)) from the same strain (44/76) in whole blood anticoagulated with the recombinant hirudin analogue. Complement activation products (C1rs-C1 inhibitor complexes, C4d, C3bBbP, and terminal SC5b-9 complex) were measured by double-antibody EIAs. Nm-LPS was a weak complement activator. Complement activation increased with preparations containing nOMVs, dOMVs, and wild-type bacteria at constant LPS concentrations. With the same protein concentration, complement activation induced by nOMVs, dOMVs, and the LPS-free mutant was equal. The massive complement activation observed in patients with fulminant meningococcal septicemia is, presumably, an indirect effect of the massive endotoxemia. Outer membrane proteins may be more potent complement activators than meningococcal LPSs.

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