Neuronal injury mediated via stimulation of microglial toll-like
receptor-9 (TLR9)
A. Iliev, A. Stringaris, R. Nau, and H. Neumann. FASEB J, 18 (2):
412-4(February 2004)Iliev, Asparouh I Stringaris, Argyrios K Nau, Roland Neumann, Harald
In Vitro United States The FASEB journal : official publication of
the Federation of American Societies for Experimental Biology FASEB
J. 2004 Feb;18(2):412-4. Epub 2003 Dec 19..
Abstract
Innate immune cells express toll-like receptor-9 (TLR9) and respond
to unmethylated, CG dinucleotide motif-rich DNA released from bacteria
during infection or endogenous cells during autoimmune tissue injury.
Oligonucleotides containing CG dinucleotide (CpG-DNA) mimic the effect
of unmethylated DNA and stimulate TLR9. CpG-DNA was cytotoxic to
neurons in organotypic brain cultures. Neurotoxicity of CpG-DNA was
mediated via microglial cells and started primarily from neurites
as determined by time-lapse imaging of enhanced green fluorescent
protein (EGFP)-transfected neurons. Cultured brain microglial cells
expressed TLR9 and responded to CpG-DNA by production of the inflammatory
mediators nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha).
Blockade of NO synthase and TNF-alpha prevented damage of neurites
and neurotoxicity of CpG-DNA. The data suggest that stimulation of
microglia via TLR9 and subsequent release of NO and TNF-alpha is
a major source of neurotoxicity in bacterial and autoimmune brain
tissue injury.
Iliev, Asparouh I Stringaris, Argyrios K Nau, Roland Neumann, Harald
In Vitro United States The FASEB journal : official publication of
the Federation of American Societies for Experimental Biology FASEB
J. 2004 Feb;18(2):412-4. Epub 2003 Dec 19.
%0 Journal Article
%1 Iliev2004
%A Iliev, A. I.
%A Stringaris, A. K.
%A Nau, R.
%A Neumann, H.
%D 2004
%J FASEB J
%K 9 Biological Cell Cerebral Cortex/drug CpG Cultured DNA DNA-Binding DNA/genetics/toxicity Factor-alpha/metabolism Hippocampus/drug Islands/genetics Methylation Microglia/cytology/drug Models, Necrosis Neurites/drug Neurons/drug Nitric Oligonucleotides/genetics/toxicity Oxide/metabolism Receptor Surface/*metabolism Toll-Like Tumor effects/*metabolism effects/*metabolism/*pathology effects/metabolism/pathology effects/pathology Proteins/metabolism
%N 2
%P 412-4
%T Neuronal injury mediated via stimulation of microglial toll-like
receptor-9 (TLR9)
%U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14688201
%V 18
%X Innate immune cells express toll-like receptor-9 (TLR9) and respond
to unmethylated, CG dinucleotide motif-rich DNA released from bacteria
during infection or endogenous cells during autoimmune tissue injury.
Oligonucleotides containing CG dinucleotide (CpG-DNA) mimic the effect
of unmethylated DNA and stimulate TLR9. CpG-DNA was cytotoxic to
neurons in organotypic brain cultures. Neurotoxicity of CpG-DNA was
mediated via microglial cells and started primarily from neurites
as determined by time-lapse imaging of enhanced green fluorescent
protein (EGFP)-transfected neurons. Cultured brain microglial cells
expressed TLR9 and responded to CpG-DNA by production of the inflammatory
mediators nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha).
Blockade of NO synthase and TNF-alpha prevented damage of neurites
and neurotoxicity of CpG-DNA. The data suggest that stimulation of
microglia via TLR9 and subsequent release of NO and TNF-alpha is
a major source of neurotoxicity in bacterial and autoimmune brain
tissue injury.
@article{Iliev2004,
abstract = {Innate immune cells express toll-like receptor-9 (TLR9) and respond
to unmethylated, CG dinucleotide motif-rich DNA released from bacteria
during infection or endogenous cells during autoimmune tissue injury.
Oligonucleotides containing CG dinucleotide (CpG-DNA) mimic the effect
of unmethylated DNA and stimulate TLR9. CpG-DNA was cytotoxic to
neurons in organotypic brain cultures. Neurotoxicity of CpG-DNA was
mediated via microglial cells and started primarily from neurites
as determined by time-lapse imaging of enhanced green fluorescent
protein (EGFP)-transfected neurons. Cultured brain microglial cells
expressed TLR9 and responded to CpG-DNA by production of the inflammatory
mediators nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha).
Blockade of NO synthase and TNF-alpha prevented damage of neurites
and neurotoxicity of CpG-DNA. The data suggest that stimulation of
microglia via TLR9 and subsequent release of NO and TNF-alpha is
a major source of neurotoxicity in bacterial and autoimmune brain
tissue injury.},
added-at = {2010-12-14T18:12:02.000+0100},
author = {Iliev, A. I. and Stringaris, A. K. and Nau, R. and Neumann, H.},
biburl = {https://www.bibsonomy.org/bibtex/252c8ea09c133d59dcba345aeb9f87813/pharmawuerz},
endnotereftype = {Journal Article},
interhash = {f4c3252f198a5c0454dbd7a798c12c44},
intrahash = {52c8ea09c133d59dcba345aeb9f87813},
issn = {1530-6860 (Electronic) 1530-6860 (Linking)},
journal = {FASEB J},
keywords = {9 Biological Cell Cerebral Cortex/drug CpG Cultured DNA DNA-Binding DNA/genetics/toxicity Factor-alpha/metabolism Hippocampus/drug Islands/genetics Methylation Microglia/cytology/drug Models, Necrosis Neurites/drug Neurons/drug Nitric Oligonucleotides/genetics/toxicity Oxide/metabolism Receptor Surface/*metabolism Toll-Like Tumor effects/*metabolism effects/*metabolism/*pathology effects/metabolism/pathology effects/pathology Proteins/metabolism},
month = Feb,
note = {Iliev, Asparouh I Stringaris, Argyrios K Nau, Roland Neumann, Harald
In Vitro United States The FASEB journal : official publication of
the Federation of American Societies for Experimental Biology FASEB
J. 2004 Feb;18(2):412-4. Epub 2003 Dec 19.},
number = 2,
pages = {412-4},
shorttitle = {Neuronal injury mediated via stimulation of microglial toll-like receptor-9
(TLR9)},
timestamp = {2010-12-14T18:21:42.000+0100},
title = {Neuronal injury mediated via stimulation of microglial toll-like
receptor-9 (TLR9)},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14688201},
volume = 18,
year = 2004
}