To cause meningitis the extracellular pathogen Neisseria meningitidis has to traverse the blood-cerebrospinal fluid (B-CSF) barrier. Postulating a transcellular passage, meningococci (MC) have been shown to adhere to and enter B-CSF barrier forming human brain microvascular endothelial cells (HBMEC). Furthermore, electron microscopy studies demonstrated that intracellular MC reside within membrane-bound compartments, both solitary and in groups. To investigate the ability of MC to survive and replicate intracellularly, prolonged gentamicin protection assays were performed. Encapsulated bacteria were found to survive and, after an initial delay, to replicate within HBMEC, whereas the number of intracellular capsule-deficient mutants decreased continuously. This strongly suggests that the capsule plays a pivotal role in the intracellular survival of MC. Further investigations were initiated to characterise the membrane-bound compartment, the Neisseria-containing vacuole (NCV). Immunfluorescence microscopy studies showed that NCVs interact with the endocytic pathway acquiring the early endosomal marker protein, transferrin receptor (TfR), and the late endosomal/lysosomal marker protein Lamp-1.
%0 Journal Article
%1 nikulin_intracellular_2006
%A Nikulin, Joanna
%A Panzner, Ursula
%A Frosch, Matthias
%A Schubert-Unkmeir, Alexandra
%D 2006
%J International Journal of Medical Microbiology: IJMM
%K 1, Brain, Electron, Endothelium, Factors Humans, Membrane Microscopy, Neisseria Protein Receptors, Replication, Signal Time Transduction, Transferrin, Vascular, ag_unkmeir meningitidis, {DNA} {Lysosomal-Associated}
%N 8
%P 553--558
%R 10.1016/j.ijmm.2006.06.006
%T Intracellular survival and replication of Neisseria meningitidis in human brain microvascular endothelial cells
%U http://www.ncbi.nlm.nih.gov/pubmed/17010667
%V 296
%X To cause meningitis the extracellular pathogen Neisseria meningitidis has to traverse the blood-cerebrospinal fluid (B-CSF) barrier. Postulating a transcellular passage, meningococci (MC) have been shown to adhere to and enter B-CSF barrier forming human brain microvascular endothelial cells (HBMEC). Furthermore, electron microscopy studies demonstrated that intracellular MC reside within membrane-bound compartments, both solitary and in groups. To investigate the ability of MC to survive and replicate intracellularly, prolonged gentamicin protection assays were performed. Encapsulated bacteria were found to survive and, after an initial delay, to replicate within HBMEC, whereas the number of intracellular capsule-deficient mutants decreased continuously. This strongly suggests that the capsule plays a pivotal role in the intracellular survival of MC. Further investigations were initiated to characterise the membrane-bound compartment, the Neisseria-containing vacuole (NCV). Immunfluorescence microscopy studies showed that NCVs interact with the endocytic pathway acquiring the early endosomal marker protein, transferrin receptor (TfR), and the late endosomal/lysosomal marker protein Lamp-1.
@article{nikulin_intracellular_2006,
abstract = {To cause meningitis the extracellular pathogen Neisseria meningitidis has to traverse the blood-cerebrospinal fluid {(B-CSF)} barrier. Postulating a transcellular passage, meningococci {(MC)} have been shown to adhere to and enter {B-CSF} barrier forming human brain microvascular endothelial cells {(HBMEC).} Furthermore, electron microscopy studies demonstrated that intracellular {MC} reside within membrane-bound compartments, both solitary and in groups. To investigate the ability of {MC} to survive and replicate intracellularly, prolonged gentamicin protection assays were performed. Encapsulated bacteria were found to survive and, after an initial delay, to replicate within {HBMEC,} whereas the number of intracellular capsule-deficient mutants decreased continuously. This strongly suggests that the capsule plays a pivotal role in the intracellular survival of {MC.} Further investigations were initiated to characterise the membrane-bound compartment, the Neisseria-containing vacuole {(NCV).} Immunfluorescence microscopy studies showed that {NCVs} interact with the endocytic pathway acquiring the early endosomal marker protein, transferrin receptor {(TfR),} and the late endosomal/lysosomal marker protein Lamp-1.},
added-at = {2011-04-07T15:44:20.000+0200},
author = {Nikulin, Joanna and Panzner, Ursula and Frosch, Matthias and {Schubert-Unkmeir}, Alexandra},
biburl = {https://www.bibsonomy.org/bibtex/2395f476ae1e137ecf635b036f358ca7f/hymi},
doi = {10.1016/j.ijmm.2006.06.006},
interhash = {e3a072f20ded4c22af876f908d76b4e5},
intrahash = {395f476ae1e137ecf635b036f358ca7f},
issn = {1438-4221},
journal = {International Journal of Medical Microbiology: {IJMM}},
keywords = {1, Brain, Electron, Endothelium, Factors Humans, Membrane Microscopy, Neisseria Protein Receptors, Replication, Signal Time Transduction, Transferrin, Vascular, ag_unkmeir meningitidis, {DNA} {Lysosomal-Associated}},
month = dec,
note = {{PMID:} 17010667},
number = 8,
pages = {553--558},
timestamp = {2011-04-07T16:38:33.000+0200},
title = {Intracellular survival and replication of Neisseria meningitidis in human brain microvascular endothelial cells},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17010667},
volume = 296,
year = 2006
}