期刊
NATURE MEDICINE
卷 20, 期 7, 页码 725-731出版社
NATURE PORTFOLIO
DOI: 10.1038/nm.3563
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资金
- Universite Paris Diderot
- La Ville de Paris
- Agence Nationale de la Recherche of France [ANR-06-MIME-029, ANR-09-BLAN-0137-03]
- Universite Paris Descartes [AAP-2011]
- Fondation pour la Recherche Medicale of France
- ANR [ANR-10-EQPX-04-01]
- Association pour la Recherche sur le Cancer
- Agence Nationale de la Recherche (ANR) [ANR-09-BLAN-0137] Funding Source: Agence Nationale de la Recherche (ANR)
Neisseria meningitidis is a cause of meningitis epidemics worldwide and of rapidly progressing fatal septic shock. A crucial step in the pathogenesis of invasive meningococcal infections is the adhesion of bloodborne meningococci to both peripheral and brain endothelia, leading to major vascular dysfunction. Initial adhesion of pathogenic strains to endothelial cells relies on meningococcal type IV pili, but the endothelial receptor for bacterial adhesion remains unknown. Here, we report that the immunoglobulin superfamily member CD147 (also called extracellular matrix metalloproteinase inducer (EMMPRIN) or Basigin) is a critical host receptor for the meningococcal pilus components PiIE and PiIV. Interfering with this interaction potently inhibited the primary attachment of meningococci to human endothelial cells in vitro and prevented colonization of vessels in human brain tissue explants ex vivo and in humanized mice in vivo. These findings establish the molecular events by which meningococci target human endothelia, and they open new perspectives for treatment and prevention of meningococcus-induced vascular dysfunctions.
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