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Complement activation and complement-dependent inflammation by Neisseria meningitidis are independent of

Tom Sprong1, Anne-Sophie W Møller, Anna Bjerre

  • 1Department of General Internal Medicine, University Medical Centre St. Radboud Nijmegen, Nijmegen, The Netherlands. t.sprong@aig.umcn.nl

Infection and Immunity
|May 25, 2004
PubMed

Insights

Meningococcal sepsis involves inflammation. This study found complement activation and immediate inflammatory effects occur independently of lipopolysaccharide (LPS), though some cytokine production relies on LPS.

Area of Science:

  • Immunology
  • Microbiology
  • Pathogenesis of Sepsis

Background:

  • Fulminant meningococcal sepsis is a model for lipopolysaccharide (LPS)-mediated gram-negative septic shock.
  • Systemic inflammation involving complement and cytokines is crucial in sepsis pathogenesis.

Purpose of the Study:

  • To investigate the role of meningococcal LPS in complement activation, inflammatory effects, and cytokine/chemokine production.
  • To differentiate LPS-dependent and LPS-independent inflammatory pathways in meningococcal sepsis.

Main Methods:

  • Whole blood was stimulated with wild-type, LPS-deficient Neisseria meningitidis, or purified meningococcal LPS.
  • Complement activation, cytokine/chemokine levels, granulocyte CR3 upregulation, and oxidative burst were measured.

Main Results:

  • Both wild-type and LPS-deficient meningococci activated complement comparably.
  • Purified LPS alone did not activate complement.
  • CR3 upregulation and oxidative burst occurred independently of LPS.
  • IL-1beta, TNF-alpha, and MIP-1alpha production were LPS-dependent, while IL-8 production was also induced by LPS-deficient bacteria.

Conclusions:

  • Complement activation and immediate inflammatory responses in meningococcal sepsis are LPS-independent.
  • Certain cytokine productions are LPS-dependent, highlighting complex inflammatory mechanisms in sepsis.

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