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Peripheral blood vessels are a niche for blood-borne meningococci

Elena Capel1,2, Jean-Philippe Barnier1,2,3, Aldert L Zomer4

  • 1a Institut Necker Enfants-Malades, INSERM U1151, Equipe 11 , Paris , France.

Virulence
|November 4, 2017
PubMed

Insights

Neisseria meningitidis colonization of human blood vessels is essential for sepsis and death. Human endothelial cells act as nutrient sources, enabling bacterial adaptation and sustained bacteremia.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Infectious Diseases

Background:

  • Neisseria meningitidis causes meningitis and purpura fulminans.
  • Bacterial adhesion to endothelial cells is key in meningococcemia.
  • Host specificity limits understanding of blood vessel colonization's role.

Purpose of the Study:

  • To investigate the role of blood vessel colonization in N. meningitidis pathogenesis.
  • To identify molecular virulence factors using a humanized mouse model.
  • To elucidate the metabolic adaptations of N. meningitidis during human endothelial cell colonization.

Main Methods:

  • Utilized a humanized SCID mouse model for in vivo studies.
  • Employed transposon insertion site sequencing (Tn-seq) to identify virulence genes.
  • Analyzed bacterial gene requirements for growth in mouse blood versus human blood vessels.

Main Results:

  • Demonstrated that meningococcal colonization of human blood vessels is critical for sepsis and lethality.
  • Found that 36% of genes essential for growth in mouse blood are dispensable for human blood vessel colonization.
  • Identified human endothelial cells as nutrient-rich niches for N. meningitidis.

Conclusions:

  • Proposes a new model for meningococcal virulence centered on blood vessel colonization.
  • Highlights metabolic adaptation to human endothelial cells as a key virulence strategy.
  • Links sustained bacteremia, driven by endothelial cell colonization, to sepsis and fatality.
Keywords:
Neisseria meningitidisTn-seqhost cell interactionnutritional virulencepurpura fulminans

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