%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 }