The endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid modulates amyloid-β-induced inflammation in BV-2 microglial cells
Abstract Amyloid-β has been shown to interact with the α7 nicotinic acetylcholine receptor on neuronal cells. Not much is known on the effect on microglial cells and whether this effect can be modulated by the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our aim was to i...
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| Published in | Journal of the neurological sciences Vol. 344; no. 1; pp. 94 - 99 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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Netherlands
Elsevier B.V
15.09.2014
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| Abstract | Abstract Amyloid-β has been shown to interact with the α7 nicotinic acetylcholine receptor on neuronal cells. Not much is known on the effect on microglial cells and whether this effect can be modulated by the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our aim was to investigate the effect of kynurenic acid on amyloid-β-treated BV-2 microglial cells with respect to α7 nicotinic acetylcholine receptor expression, cell viability, cytokine production and phagocytotic abilities. Therefore BV-2 cells were treated with oligomeric or fibrillar forms of amyloid-β1–40 and co-treated with kynurenic acid. α7 nicotinic acetylcholine receptor quantity was investigated using Western blotting. Cell viability was assessed by staining cells with fluorescein diacetate and propidium iodide. Pro-inflammatory cytokines were measured in cell culture supernatants of treated cells with ELISAs; NO with Griess reagents and amyloid-β uptake were investigated with fluorescence-activated cell sorting and verified by Western blotting. Amyloid-β nor kynurenic acid did have an effect on the protein level of the α7 nicotinic acetylcholine receptor. Amyloid-Beta induced cell mortality was unchanged after addition of kynurenic acid. However, kynurenic acid co-treatment reduced the pro-inflammatory cytokines tumour necrosis factor-α and IL-6 and amyloid-β phagocytosis. We provide evidence for an immunomodulating effect of the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our findings indicate a role for kynurenic acid in amyloid-β associated neuroinflammation in Alzheimer disease. |
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| AbstractList | Amyloid-β has been shown to interact with the α7 nicotinic acetylcholine receptor on neuronal cells. Not much is known on the effect on microglial cells and whether this effect can be modulated by the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our aim was to investigate the effect of kynurenic acid on amyloid-β-treated BV-2 microglial cells with respect to α7 nicotinic acetylcholine receptor expression, cell viability, cytokine production and phagocytotic abilities. Therefore BV-2 cells were treated with oligomeric or fibrillar forms of amyloid-β1–40 and co-treated with kynurenic acid. α7 nicotinic acetylcholine receptor quantity was investigated using Western blotting. Cell viability was assessed by staining cells with fluorescein diacetate and propidium iodide. Pro-inflammatory cytokines were measured in cell culture supernatants of treated cells with ELISAs; NO with Griess reagents and amyloid-β uptake were investigated with fluorescence-activated cell sorting and verified by Western blotting. Amyloid-β nor kynurenic acid did have an effect on the protein level of the α7 nicotinic acetylcholine receptor. Amyloid-Beta induced cell mortality was unchanged after addition of kynurenic acid. However, kynurenic acid co-treatment reduced the pro-inflammatory cytokines tumour necrosis factor-α and IL-6 and amyloid-β phagocytosis.
We provide evidence for an immunomodulating effect of the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our findings indicate a role for kynurenic acid in amyloid-β associated neuroinflammation in Alzheimer disease.
•Kynurenic acid and amyloid-β do not change α7nAchR quantity on BV-2 microglial cells•Kynurenic acid reduces amyloid-β induced pro-inflammatory cytokines TNF-α and IL-6.•Kynurenic acid decreases amyloid-β phagocytosis in BV-2 microglial cells Amyloid-β has been shown to interact with the α7 nicotinic acetylcholine receptor on neuronal cells. Not much is known on the effect on microglial cells and whether this effect can be modulated by the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our aim was to investigate the effect of kynurenic acid on amyloid-β-treated BV-2 microglial cells with respect to α7 nicotinic acetylcholine receptor expression, cell viability, cytokine production and phagocytotic abilities. Therefore BV-2 cells were treated with oligomeric or fibrillar forms of amyloid-β(1-40) and co-treated with kynurenic acid. α7 nicotinic acetylcholine receptor quantity was investigated using Western blotting. Cell viability was assessed by staining cells with fluorescein diacetate and propidium iodide. Pro-inflammatory cytokines were measured in cell culture supernatants of treated cells with ELISAs; NO with Griess reagents and amyloid-β uptake were investigated with fluorescence-activated cell sorting and verified by Western blotting. Amyloid-β nor kynurenic acid did have an effect on the protein level of the α7 nicotinic acetylcholine receptor. Amyloid-Beta induced cell mortality was unchanged after addition of kynurenic acid. However, kynurenic acid co-treatment reduced the pro-inflammatory cytokines tumour necrosis factor-α and IL-6 and amyloid-β phagocytosis. We provide evidence for an immunomodulating effect of the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our findings indicate a role for kynurenic acid in amyloid-β associated neuroinflammation in Alzheimer disease. Abstract Amyloid-β has been shown to interact with the α7 nicotinic acetylcholine receptor on neuronal cells. Not much is known on the effect on microglial cells and whether this effect can be modulated by the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our aim was to investigate the effect of kynurenic acid on amyloid-β-treated BV-2 microglial cells with respect to α7 nicotinic acetylcholine receptor expression, cell viability, cytokine production and phagocytotic abilities. Therefore BV-2 cells were treated with oligomeric or fibrillar forms of amyloid-β1–40 and co-treated with kynurenic acid. α7 nicotinic acetylcholine receptor quantity was investigated using Western blotting. Cell viability was assessed by staining cells with fluorescein diacetate and propidium iodide. Pro-inflammatory cytokines were measured in cell culture supernatants of treated cells with ELISAs; NO with Griess reagents and amyloid-β uptake were investigated with fluorescence-activated cell sorting and verified by Western blotting. Amyloid-β nor kynurenic acid did have an effect on the protein level of the α7 nicotinic acetylcholine receptor. Amyloid-Beta induced cell mortality was unchanged after addition of kynurenic acid. However, kynurenic acid co-treatment reduced the pro-inflammatory cytokines tumour necrosis factor-α and IL-6 and amyloid-β phagocytosis. We provide evidence for an immunomodulating effect of the endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid. Our findings indicate a role for kynurenic acid in amyloid-β associated neuroinflammation in Alzheimer disease. |
| Author | Mengel, David Gold, Maike Steiner, Levke Dodel, Richard Bach, Jan-Philipp |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25064444$$D View this record in MEDLINE/PubMed |
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| Keywords | FDA KYNA Alzheimer disease DMSO Interleukin quinolinic acid fluorescence-activated cell sorting FACS fluorescein diacetate TNF sodium dodecyl sulphate-polyacrylamide gel-electrophoresis QA Aβ FITC dimethyl sulfoxide propidium iodide FBS fluorescein isothiocyanate PBS AD IL amyloid-β Inflammation Microglia fetal bovine serum SDS-PAGE α7nAChR phosphate buffered saline enzyme-linked immunosorbent assay PI tumour necrosis factor GAPDH kynurenic acid Phagocytosis α7 nicotinic acetylcholine receptor ELISA glyceraldehyde 3-phosphate dehydrogenase Kynurenic acid |
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| Snippet | Abstract Amyloid-β has been shown to interact with the α7 nicotinic acetylcholine receptor on neuronal cells. Not much is known on the effect on microglial... Amyloid-β has been shown to interact with the α7 nicotinic acetylcholine receptor on neuronal cells. Not much is known on the effect on microglial cells and... |
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| SubjectTerms | alpha7 Nicotinic Acetylcholine Receptor - antagonists & inhibitors alpha7 Nicotinic Acetylcholine Receptor - metabolism Alzheimer disease Amyloid beta-Peptides - pharmacology Animals Cell Line, Transformed Cell Survival Dose-Response Relationship, Drug Enzyme-Linked Immunosorbent Assay Excitatory Amino Acid Antagonists Inflammation Interleukin-6 - metabolism Kynurenic acid Kynurenic Acid - pharmacology Mice Mice, Inbred C57BL Microglia Microglia - drug effects Neurology Nitric Oxide - metabolism Peptide Fragments - pharmacology Phagocytosis Phagocytosis - drug effects Tumor Necrosis Factor-alpha - metabolism α7 nicotinic acetylcholine receptor |
| Title | The endogenous α7 nicotinic acetylcholine receptor antagonist kynurenic acid modulates amyloid-β-induced inflammation in BV-2 microglial cells |
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