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Neisseria meningitidis induces platelet inhibition and increases vascular endothelial permeability via nitric oxide

Anna Kobsar1, Celine Siauw, Stepan Gambaryan

  • 1Institute of Clinical Biochemistry and Pathobiochemistry /Central Laboratory, University of Wuerzburg, Germany.

Thrombosis and Haemostasis
|November 11, 2011
PubMed

Insights

Neisseria meningitidis produces nitric oxide (NO), a molecule that inhibits platelet aggregation and increases blood vessel permeability. This NO production is crucial in the severe symptoms of meningococcal sepsis, including Waterhouse-Friderichsen syndrome.

Area of Science:

  • Microbiology
  • Vascular Biology
  • Pathophysiology

Background:

  • Neisseria meningitidis infections cause high morbidity and mortality despite antibiotics.
  • Fulminant meningococcal sepsis (Waterhouse-Friderichsen syndrome) involves adrenal hemorrhage and bleeding, suggesting platelet dysfunction.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) produced by N. meningitidis in the pathophysiology of meningococcal infections.
  • To determine the effects of bacterial NO on platelet function and endothelial cell permeability.

Main Methods:

  • Measurement of NO production by N. meningitidis.
  • Assay of ADP-induced platelet aggregation and cyclic nucleotide levels.
  • Assessment of endothelial cell monolayer permeability using horseradish peroxidase (HRP) passage.
  • Immunofluorescence analysis of endothelial adherens junctions.

Main Results:

  • N. meningitidis produces nitric oxide (NO).
  • Bacterial NO inhibits ADP-induced platelet aggregation via soluble guanylyl cyclase (sGC) and cyclic nucleotide-dependent protein kinases (PKG, PKA).
  • N. meningitidis increases endothelial monolayer permeability, with NO-dependent disruption of adherens junctions, independent of cyclic nucleotides.

Conclusions:

  • Nitric oxide (NO) produced by N. meningitidis plays a significant role in the pathophysiology of meningococcal sepsis.
  • Bacterial NO contributes to platelet inhibition and increased vascular permeability, exacerbating disease severity.

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