Priming of microglia by type II interferon is lasting and resistant to modulation by interleukin-10 in situ
Immunological priming by type II interferon (IFN-γ) is crucial for evoking neurotoxic phenotypes of microglia (tissue-resident macrophages). We report that serial exposure of hippocampal slice cultures to IFN-γ and lipopolysaccharide (Toll-like receptor 4 ligand) induces high release of IL-6, TNF-α...
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| Hauptverfasser: | , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
28 April 2022
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| In: |
Journal of neuroimmunology
Year: 2022, Jahrgang: 368, Pages: 1-10 |
| ISSN: | 1872-8421 |
| DOI: | 10.1016/j.jneuroim.2022.577881 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.jneuroim.2022.577881 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0165572822000765 
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| Verfasserangaben: | Marc Hemmerich, Nikolai Malorny, Andrea Lewen, Jan-Oliver Hollnagel, Bruno Chausse, Oliver Kann |
MARC
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| 520 | |a Immunological priming by type II interferon (IFN-γ) is crucial for evoking neurotoxic phenotypes of microglia (tissue-resident macrophages). We report that serial exposure of hippocampal slice cultures to IFN-γ and lipopolysaccharide (Toll-like receptor 4 ligand) induces high release of IL-6, TNF-α and nitric oxide, concomitant loss of electrical network activity (neuronal gamma oscillations) and neurodegeneration. Notably, these effects are still present after 3 days of IFN-γ removal but neither mimicked by IFN-α nor attenuated by anti-inflammatory cytokine, IL-10. Our findings might be relevant for brain diseases featuring elevated IFN-γ levels, such as viral and bacterial infections, multiple sclerosis and Alzheimer's disease. | ||
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