Invasive meningococcal disease: a disease of the endothelial cells

Mathieu Coureuil1, Sandrine Bourdoulous2, Stefano Marullo2

  • 1Institut Necker-Enfants Malades, 14, rue Maria Helena Vieira Da Silva, CS 61431, 75014 Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Paris, France; INSERM U1151 and U1016, Paris, France; CNRS UMR 8253 and UMR 8104, Paris, France.

Insights

Neisseria meningitidis uses type IV pili to adhere to endothelial cells via CD147 and the β2-adrenoceptor. This interaction causes meningitis and vascular leakage, leading to severe infections like purpura fulminans.

Area of Science:

  • Microbiology
  • Pathogen-host interactions
  • Infectious diseases

Background:

  • Neisseria meningitidis is an extracellular bacterium causing invasive infections.
  • Meningococcal adhesion to endothelial cells is crucial for disease pathogenesis.
  • Understanding these interactions informs treatment strategies.

Purpose of the Study:

  • To review the mechanisms of Neisseria meningitidis interaction with endothelial cells.
  • To elucidate the role of CD147 and β2-adrenoceptor in meningococcal disease.
  • To connect pathogen-endothelial interactions with clinical manifestations.

Main Methods:

  • Literature review of pathogen-host interactions.
  • Analysis of bacterial virulence factors (type IV pili).
  • Examination of endothelial cell receptors (CD147, β2-adrenoceptor).

Main Results:

  • Neisseria meningitidis forms microcolonies on endothelium via type IV pili.
  • CD147 mediates bacterial adhesion; β2-adrenoceptor facilitates signaling and BBB crossing.
  • These interactions are linked to meningitis and vascular leakage syndromes.

Conclusions:

  • Meningococcal interaction with endothelial cells drives key clinical features of invasive disease.
  • Targeting pathogen-adhesion mechanisms may offer therapeutic potential.
  • Further research into these interactions is vital for combating meningococcal infections.

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