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Trends Mol Med. 2014 Oct;20(10):571-8. doi: 10.1016/j.molmed.2014.08.002. Epub 2014 Aug 29.

Invasive meningococcal disease: a disease of the endothelial cells.

Author information

1
Institut 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.
2
Université Paris Descartes, Sorbonne Paris Cité, Paris, France; INSERM U1151 and U1016, Paris, France; CNRS UMR 8253 and UMR 8104, Paris, France; Institut Cochin, 22 rue Méchin, 75014 Paris, France.
3
Institut 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. Electronic address: xavier.nassif@inserm.fr.

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.

KEYWORDS:

CD147; Neisseria meningitidis; endothelium; meningitis; purpura fulminans; β2-adrenoceptor

PMID:
25178566
DOI:
10.1016/j.molmed.2014.08.002
[Indexed for MEDLINE]

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