Mechanism of meningeal invasion by Neisseria meningitidis

The blood-cerebrospinal fluid barrier physiologically protects the meningeal spaces from blood-borne bacterial pathogens, due to the existence of specialized junctional interendothelial complexes. Few bacterial pathogens are able to reach the subarachnoidal space and among those, Neisseria meningiti...

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Published inVirulence Vol. 3; no. 2; pp. 164 - 172
Main Authors Coureuil, Mathieu, Join-Lambert, Olivier, Lécuyer, Hervé, Bourdoulous, Sandrine, Marullo, Stefano, Nassif, Xavier
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 01.03.2012
Landes Bioscience
Subjects
beta 2 adrenergic receptor
Binding
Biology
Bioscience
blood-brain barrier
Blood-Brain Barrier - immunology
Blood-Brain Barrier - microbiology
brain endothelial cells
Calcium
Cancer
Cell
central nervous system infections
cerebrospinal meningitis
Cycle
Endothelial Cells - microbiology
Fimbriae, Bacterial - metabolism
Host-Pathogen Interactions
Humans
Landes
Meningitis, Meningococcal - microbiology
Meningitis, Meningococcal - pathology
neisseria meningitidis
Neisseria meningitidis - immunology
Neisseria meningitidis - pathogenicity
Organogenesis
Proteins
Review
Virulence
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Abstract The blood-cerebrospinal fluid barrier physiologically protects the meningeal spaces from blood-borne bacterial pathogens, due to the existence of specialized junctional interendothelial complexes. Few bacterial pathogens are able to reach the subarachnoidal space and among those, Neisseria meningitidis is the one that achieves this task the most constantly when present in the bloodstream. Meningeal invasion is a consequence of a tight interaction of meningococci with brain endothelial cells. This interaction, mediated by the type IV pili, is responsible for the formation of microcolonies on the apical surface of the cells. This interaction is followed by the activation of signaling pathways in the host cells leading to the formation of endothelial docking structures resembling those elicited by the interaction of leukocytes with endothelial cells during extravasation. The consequence of these bacterial-induced signaling events is the recruitment of intercellular junction components in the docking structure and the subsequent opening of the intercellular junctions.
AbstractList The blood-cerebrospinal fluid barrier physiologically protects the meningeal spaces from blood-borne bacterial pathogens, due to the existence of specialized junctional interendothelial complexes. Few bacterial pathogens are able to reach the subarachnoidal space and among those, Neisseria meningitidis is the one that achieves this task the most constantly when present in the bloodstream. Meningeal invasion is a consequence of a tight interaction of meningococci with brain endothelial cells. This interaction, mediated by the type IV pili, is responsible for the formation of microcolonies on the apical surface of the cells. This interaction is followed by the activation of signaling pathways in the host cells leading to the formation of endothelial docking structures resembling those elicited by the interaction of leukocytes with endothelial cells during extravasation. The consequence of these bacterial-induced signaling events is the recruitment of intercellular junction components in the docking structure and the subsequent opening of the intercellular junctions.
The blood-cerebrospinal fluid barrier physiologically protects the meningeal spaces from blood-borne bacterial pathogens, due to the existence of specialized junctional interendothelial complexes. Few bacterial pathogens are able to reach the subarachnoidal space and among those, Neisseria meningitidis is the one that achieves this task the most constantly when present in the bloodstream. Meningeal invasion is a consequence of a tight interaction of meningococci with brain endothelial cells. This interaction, mediated by the type IV pili, is responsible for the formation of microcolonies on the apical surface of the cells. This interaction is followed by the activation of signaling pathways in the host cells leading to the formation of endothelial docking structures resembling those elicited by the interaction of leukocytes with endothelial cells during extravasation. The consequence of these bacterial-induced signaling events is the recruitment of intercellular junction components in the docking structure and the subsequent opening of the intercellular junctions.
Author Bourdoulous, Sandrine
Marullo, Stefano
Join-Lambert, Olivier
Nassif, Xavier
Lécuyer, Hervé
Coureuil, Mathieu
AuthorAffiliation Université Paris Descartes; Sorbonne Paris Cité; Faculté de Médecine; Paris, France
CNRS UMR8104; Paris, France
Assistance Publique; Hôpitaux de Paris; Hôpital Necker Enfants Malades; Paris, France
INSERM U1016; Institut Cochin; Paris, France
INSERM U1002; Paris, France
AuthorAffiliation_xml – name: Université Paris Descartes; Sorbonne Paris Cité; Faculté de Médecine; Paris, France
– name: INSERM U1016; Institut Cochin; Paris, France
– name: CNRS UMR8104; Paris, France
– name: Assistance Publique; Hôpitaux de Paris; Hôpital Necker Enfants Malades; Paris, France
– name: INSERM U1002; Paris, France
Author_xml – sequence: 1
  givenname: Mathieu
  surname: Coureuil
  fullname: Coureuil, Mathieu
– sequence: 2
  givenname: Olivier
  surname: Join-Lambert
  fullname: Join-Lambert, Olivier
– sequence: 3
  givenname: Hervé
  surname: Lécuyer
  fullname: Lécuyer, Hervé
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  givenname: Sandrine
  surname: Bourdoulous
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  surname: Marullo
  fullname: Marullo, Stefano
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  givenname: Xavier
  surname: Nassif
  fullname: Nassif, Xavier
  email: xavier.nassif@inserm.fr
BackLink https://www.ncbi.nlm.nih.gov/pubmed/22366962$$D View this record in MEDLINE/PubMed
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Snippet The blood-cerebrospinal fluid barrier physiologically protects the meningeal spaces from blood-borne bacterial pathogens, due to the existence of specialized...
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SubjectTerms beta 2 adrenergic receptor
Binding
Biology
Bioscience
blood-brain barrier
Blood-Brain Barrier - immunology
Blood-Brain Barrier - microbiology
brain endothelial cells
Calcium
Cancer
Cell
central nervous system infections
cerebrospinal meningitis
Cycle
Endothelial Cells - microbiology
Fimbriae, Bacterial - metabolism
Host-Pathogen Interactions
Humans
Landes
Meningitis, Meningococcal - microbiology
Meningitis, Meningococcal - pathology
neisseria meningitidis
Neisseria meningitidis - immunology
Neisseria meningitidis - pathogenicity
Organogenesis
Proteins
Review
Virulence
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Title Mechanism of meningeal invasion by Neisseria meningitidis
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