Home > Publications Database > NLRP3-directed antisense oligonucleotides reduce microglial immunoactivities in vitro. > print

001     257344
005     20250127091814.0
024 7 _ |a 10.1111/jnc.15778
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024 7 _ |a pmid:36799439
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024 7 _ |a 0022-3042
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024 7 _ |a 1471-4159
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037 _ _ |a DZNE-2023-00413
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Braatz, Charlotte
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245 _ _ |a NLRP3-directed antisense oligonucleotides reduce microglial immunoactivities in vitro.
260 _ _ |a Oxford
|c 2024
|b Wiley-Blackwell
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520 _ _ |a Alzheimer's disease (AD) is associated with the cerebral deposition of Amyloid-β (Aβ) peptide, which leads to NLRP3 inflammasome activation and subsequent release of interleukin-1β (IL-1β) and interleukin-18 (IL-18). NLRP3 reduction has been found to increase microglial clearance, protect from synapse loss, and suppress both the changes to synaptic plasticity and spatial memory dysfunction observed in murine AD models. Here, we test whether NLRP3-directed antisense oligonucleotides (ASOs) can be harnessed as immune modulators in primary murine microglia and human THP-1 cells. NLRP3 mRNA degradation was achieved at 72 h of ASO treatment in primary murine microglia. Consequently, NLRP3-directed ASOs significantly reduced the levels of cleaved caspase-1 and mature IL-1β when microglia were either activated by LPS and nigericin or LPS and Aβ. In human THP-1 cells NLRP3-targeted ASOs also significantly reduced the LPS plus nigericin- or LPS plus Aβ-induced release of mature IL-1β. Together, NLRP3-directed ASOs can suppress NLRP3 inflammasome activity and subsequent release of IL-1β in primary murine microglia and THP-1 cells. ASOs may represent a new and alternative approach to modulate NLRP3 inflammasome activation in neurodegenerative diseases, in addition to attempts to inhibit the complex pharmacologically.
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650 _ 7 |a Alzheimer's disease
|2 Other
650 _ 7 |a Aβ
|2 Other
650 _ 7 |a NLRP3 inflammasome
|2 Other
650 _ 7 |a antisense oligonucleotides
|2 Other
650 _ 7 |a innate immunity
|2 Other
650 _ 7 |a microglia
|2 Other
650 _ 7 |a neuroinflammation
|2 Other
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Microglia: drug effects
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a NLR Family, Pyrin Domain-Containing 3 Protein: metabolism
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Oligonucleotides, Antisense: pharmacology
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Interleukin-1beta: metabolism
|2 MeSH
650 _ 2 |a Inflammasomes: metabolism
|2 MeSH
650 _ 2 |a THP-1 Cells
|2 MeSH
650 _ 2 |a Cells, Cultured
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700 1 _ |a Komes, Max
|0 P:(DE-2719)9001384
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700 1 _ |a Ravichandran, Kishore
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700 1 _ |a Garcia de Fragas, Matheus
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700 1 _ |a Griep, Angelika
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700 1 _ |a Schwartz, Stephanie
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700 1 _ |a McManus, Roisin
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700 1 _ |a Heneka, Michael T
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770 _ _ |a Neuroimmunology
773 _ _ |a 10.1111/jnc.15778
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|t Journal of neurochemistry
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|y 2024
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