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Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery
Published on: November 5, 2019
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.
Abstract:
Neisseria meningitidis is an extracellular pathogen, which, once in the bloodstream, has the ability to form microcolonies on the apical surface of endothelia. Pathogen interaction with microvessels is mediated by bacterial type IV pili and two receptors on endothelial cells: CD147 and the β2-adrenoceptor. CD147 facilitates the adhesion of diplococci to the endothelium, whereas the β2-adrenoceptor facilitates cell signaling, and crossing of the blood-brain barrier. In this review, we discuss how meningococcal interaction with endothelial cells is responsible for the specific clinical features of invasive meningococcal infection such as meningitis, and a peripheral thrombotic/vascular leakage syndrome possibly leading to purpura fulminans.
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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