Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2
and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation
in primary mouse microglial cell cultures
M. Lotz, S. Ebert, H. Esselmann, A. Iliev, M. Prinz, N. Wiazewicz, J. Wiltfang, J. Gerber, and R. Nau. J Neurochem, 94 (2):
289-98(July 2005)Lotz, Miriam Ebert, Sandra Esselmann, Hermann Iliev, Asparouh I Prinz,
Marco Wiazewicz, Nicole Wiltfang, Jens Gerber, Joachim Nau, Roland
Comparative Study Research Support, Non-U.S. Gov't England Journal
of neurochemistry J Neurochem. 2005 Jul;94(2):289-98..
Abstract
The interaction of endogenous and exogenous stimulators of innate
immunity was examined in primary cultures of mouse microglial cells
and macrophages after application of defined Toll-like receptor (TLR)
agonists lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide
Pam3Cys-Ser-Lys4 (Pam3Cys) (TLR2) and single-stranded unmethylated
CpG-DNA (CpG) (TLR9) alone and in combination with amyloid beta
peptide (Abeta) 1-40. Abeta1-40 stimulated microglial cells and macrophages
primed by interferon-gamma in a dose-dependent manner. Co-administration
of Abeta1-40 with LPS or Pam3Cys led to an additive release of nitric
oxide (NO) and tumour necrosis factor alpha (TNF-alpha). This may
be one reason for the clinical deterioration frequently observed
in patients with Alzheimer's disease during infections. In contrast,
co-application of Abeta1-40 with CpG led to a substantial decrease
of NO and TNF-alpha release compared with stimulation with CpG alone.
Abeta1-40 and CpG did not co-localize within the same subcellular
compartment, making a direct physicochemical interaction as the cause
of the observed antagonism very unlikely. This suggests that not
all TLR agonists enhance the stimulatory effect of A beta on innate
immunity.
Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2
and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation
in primary mouse microglial cell cultures
Lotz, Miriam Ebert, Sandra Esselmann, Hermann Iliev, Asparouh I Prinz,
Marco Wiazewicz, Nicole Wiltfang, Jens Gerber, Joachim Nau, Roland
Comparative Study Research Support, Non-U.S. Gov't England Journal
of neurochemistry J Neurochem. 2005 Jul;94(2):289-98.
%0 Journal Article
%1 Lotz2005
%A Lotz, M.
%A Ebert, S.
%A Esselmann, H.
%A Iliev, A. I.
%A Prinz, M.
%A Wiazewicz, N.
%A Wiltfang, J.
%A Gerber, J.
%A Nau, R.
%D 2005
%J J Neurochem
%K & 2 4 9 Amyloid Analysis Animals Animals, Assay/methods Bacterial/pharmacology Blotting, Brain/cytology C57BL Cell Confocal/methods Cultured Cytokines/metabolism DNA, DNA-Binding Dose-Response Drug Enzyme-Linked Fragments/metabolism/*pharmacology Immunohistochemistry/methods Immunologic/*agonists Immunosorbent Inflammation/chemically Interactions Lectins/metabolism Lipopolysaccharides/*pharmacology Lipoproteins/*pharmacology Macrophages/drug Mice Microglia/*drug Microscopy, Newborn Nitrites/metabolism Peptide Proteins/*antagonists Receptor Relationship, Surface/*antagonists Survival/drug Toll-Like Variance Western/methods beta-Protein/metabolism/*pharmacology effects effects/physiology induced/*physiopathology inhibitors of
%N 2
%P 289-98
%T Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2
and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation
in primary mouse microglial cell cultures
%U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15998280
%V 94
%X The interaction of endogenous and exogenous stimulators of innate
immunity was examined in primary cultures of mouse microglial cells
and macrophages after application of defined Toll-like receptor (TLR)
agonists lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide
Pam3Cys-Ser-Lys4 (Pam3Cys) (TLR2) and single-stranded unmethylated
CpG-DNA (CpG) (TLR9) alone and in combination with amyloid beta
peptide (Abeta) 1-40. Abeta1-40 stimulated microglial cells and macrophages
primed by interferon-gamma in a dose-dependent manner. Co-administration
of Abeta1-40 with LPS or Pam3Cys led to an additive release of nitric
oxide (NO) and tumour necrosis factor alpha (TNF-alpha). This may
be one reason for the clinical deterioration frequently observed
in patients with Alzheimer's disease during infections. In contrast,
co-application of Abeta1-40 with CpG led to a substantial decrease
of NO and TNF-alpha release compared with stimulation with CpG alone.
Abeta1-40 and CpG did not co-localize within the same subcellular
compartment, making a direct physicochemical interaction as the cause
of the observed antagonism very unlikely. This suggests that not
all TLR agonists enhance the stimulatory effect of A beta on innate
immunity.
@article{Lotz2005,
abstract = {The interaction of endogenous and exogenous stimulators of innate
immunity was examined in primary cultures of mouse microglial cells
and macrophages after application of defined Toll-like receptor (TLR)
agonists [lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide
Pam3Cys-Ser-Lys4 (Pam3Cys) (TLR2) and single-stranded unmethylated
CpG-DNA (CpG) (TLR9)] alone and in combination with amyloid beta
peptide (Abeta) 1-40. Abeta1-40 stimulated microglial cells and macrophages
primed by interferon-gamma in a dose-dependent manner. Co-administration
of Abeta1-40 with LPS or Pam3Cys led to an additive release of nitric
oxide (NO) and tumour necrosis factor alpha (TNF-alpha). This may
be one reason for the clinical deterioration frequently observed
in patients with Alzheimer's disease during infections. In contrast,
co-application of Abeta1-40 with CpG led to a substantial decrease
of NO and TNF-alpha release compared with stimulation with CpG alone.
Abeta1-40 and CpG did not co-localize within the same subcellular
compartment, making a direct physicochemical interaction as the cause
of the observed antagonism very unlikely. This suggests that not
all TLR agonists enhance the stimulatory effect of A beta on innate
immunity.},
added-at = {2010-12-14T18:12:02.000+0100},
author = {Lotz, M. and Ebert, S. and Esselmann, H. and Iliev, A. I. and Prinz, M. and Wiazewicz, N. and Wiltfang, J. and Gerber, J. and Nau, R.},
biburl = {https://www.bibsonomy.org/bibtex/204ab8ab33c6bdf33fd35ceb0d7d332be/pharmawuerz},
endnotereftype = {Journal Article},
interhash = {f8aea642d0fda178275c420c79048bf0},
intrahash = {04ab8ab33c6bdf33fd35ceb0d7d332be},
issn = {0022-3042 (Print) 0022-3042 (Linking)},
journal = {J Neurochem},
keywords = {& 2 4 9 Amyloid Analysis Animals Animals, Assay/methods Bacterial/pharmacology Blotting, Brain/cytology C57BL Cell Confocal/methods Cultured Cytokines/metabolism DNA, DNA-Binding Dose-Response Drug Enzyme-Linked Fragments/metabolism/*pharmacology Immunohistochemistry/methods Immunologic/*agonists Immunosorbent Inflammation/chemically Interactions Lectins/metabolism Lipopolysaccharides/*pharmacology Lipoproteins/*pharmacology Macrophages/drug Mice Microglia/*drug Microscopy, Newborn Nitrites/metabolism Peptide Proteins/*antagonists Receptor Relationship, Surface/*antagonists Survival/drug Toll-Like Variance Western/methods beta-Protein/metabolism/*pharmacology effects effects/physiology induced/*physiopathology inhibitors of},
month = Jul,
note = {Lotz, Miriam Ebert, Sandra Esselmann, Hermann Iliev, Asparouh I Prinz,
Marco Wiazewicz, Nicole Wiltfang, Jens Gerber, Joachim Nau, Roland
Comparative Study Research Support, Non-U.S. Gov't England Journal
of neurochemistry J Neurochem. 2005 Jul;94(2):289-98.},
number = 2,
pages = {289-98},
shorttitle = {Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2
and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation
in primary mouse microglial cell cultures},
timestamp = {2010-12-14T18:22:14.000+0100},
title = {Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2
and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation
in primary mouse microglial cell cultures},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15998280},
volume = 94,
year = 2005
}