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Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature
Published on: April 1, 2014
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Pathogenic Neisseria meningitidis utilizes CD147 for vascular colonization
Sandra C Bernard1, Nandi Simpson2, Olivier Join-Lambert3
11] INSERM, U1016, Institut Cochin, Paris, France. [2] CNRS, UMR8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Université Paris Diderot, Paris, France. [5].
Nature Medicine
|June 2, 2014
Summary
Neisseria meningitidis uses CD147 as a receptor to attach to human endothelial cells, causing meningitis and septic shock. Blocking this interaction prevents bacterial adhesion and vessel colonization, offering new treatment strategies.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Neisseria meningitidis causes meningitis and septic shock globally.
- Bacterial adhesion to endothelial cells is critical for invasive meningococcal disease.
- The specific endothelial receptor for initial bacterial attachment is unknown.
Purpose of the Study:
- To identify the host endothelial receptor for Neisseria meningitidis adhesion.
- To investigate the role of this receptor in meningococcal pathogenesis.
- To explore therapeutic strategies targeting this interaction.
Main Methods:
- Investigated the interaction between meningococcal type IV pili (PilE, PilV) and endothelial cells.
- Utilized in vitro assays with human endothelial cells.
- Employed ex vivo human brain tissue explants and in vivo humanized mouse models.
Main Results:
- Identified CD147 (EMMPRIN/Basigin) as a critical host receptor for Neisseria meningitidis.
- Demonstrated that CD147 binds to meningococcal pilus components PilE and PilV.
- Inhibition of CD147-mediated interaction significantly reduced bacterial attachment and prevented vessel colonization.
Conclusions:
- CD147 is a key receptor mediating the adhesion of Neisseria meningitidis to human endothelia.
- Targeting the CD147-meningococcal interaction offers a novel therapeutic approach.
- Understanding this molecular mechanism provides insights into preventing meningococcus-induced vascular dysfunction.
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