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Microglial pattern recognition via IL-33 promotes synaptic refinement in developing corticothalamic circuits in mice (bulk RNA-seq)

ABSTRACT: To determine the direct effect of IL-33 on microglial gene expression, we have bulk RNA-sequenced cortical microglia 4 hours after IL-33 or vehicle i.c.v. injection.

ORGANISM(S): Mus musculus

PROVIDER: GSE218369 | GEO | 2022/12/12

REPOSITORIES: GEO

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Microglial pattern recognition via IL-33 promotes synaptic refinement in developing corticothalamic circuits in mice (ATACseq)

Project description:To determine the direct effect of IL-33 on microglial gene expression, we have bulk ATAC-sequenced cortical microglia 4 hours after IL-33 or vehicle i.c.v. injection.

2022-12-12 | GSE218424 | GEO

Microglial pattern recognition via IL-33 promotes synaptic refinement in developing corticothalamic circuits in mice (scRNAseq)

Project description:To determine the effect of IL-33 on microglial gene expression, we have scRNA-sequenced cortical microglia from ST2KO and WT mice 4 hours after IL-33 or vehicle i.c.v. injection.

2022-12-12 | GSE218427 | GEO

Microglial pattern recognition via IL-33 promotes synaptic refinement in developing corticothalamic circuits in mice (H3K27ac ChIP-seq)

Project description:To determine the direct effect of IL-33 on microglial gene expression, we have H3K27ac ChIP-sequenced cortical microglia 4 hours after IL-33 or vehicle i.c.v. injection.

2022-12-12 | GSE218426 | GEO

Microglial pattern recognition via IL-33 promotes synaptic refinement in developing corticothalamic circuits in mice (FOS ChIP-seq)

Project description:To determine whether FOS is involved in the IL-33 microglial gene expression response, we have FOS ChIP-sequenced cortical microglia 4 hours after IL-33 i.c.v. injection.

2022-12-12 | GSE218425 | GEO

Microglial pattern recognition via IL-33 promotes synaptic refinement in developing corticothalamic circuits in mice.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-12 | GSE218428 | GEO

Astrocyte-secreted IL-33 mediates homeostatic synaptic plasticity in the adult hippocampus

Project description:Hippocampal synaptic plasticity is important for learning and memory formation. Homeostatic synaptic plasticity is a specific form of synaptic plasticity that is induced upon prolonged changes in neuronal activity to maintain network homeostasis. While astrocytes are important regulators of synaptic transmission and plasticity, it is largely unclear how they interact with neurons to regulate synaptic plasticity at the circuit level. Here, we show that neuronal activity blockade selectively increases the expression and secretion of IL-33 (interleukin-33) by astrocytes in the hippocampal cornu ammonis 1 (CA1) subregion. This IL-33 stimulates an increase in excitatory synapses and neurotransmission through the activation of neuronal IL-33 receptor complex and synaptic recruitment of the scaffold protein PSD-95. We found that acute administration of tetrodotoxin in hippocampal slices or inhibition of hippocampal CA1 excitatory neurons by optogenetic manipulation increases IL-33 expression in CA1 astrocytes. Furthermore, IL-33 administration in vivo promotes the formation of functional excitatory synapses in hippocampal CA1 neurons, whereas conditional knockout of IL-33 in CA1 astrocytes decreases the number of excitatory synapses therein. Importantly, blockade of IL-33 and its receptor signaling in vivo by intracerebroventricular administration of its decoy receptor inhibits homeostatic synaptic plasticity in CA1 pyramidal neurons and impairs spatial memory formation in mice. These results collectively reveal an important role of astrocytic IL-33 in mediating the negative-feedback signaling mechanism in homeostatic synaptic plasticity, providing insights into how astrocytes maintain hippocampal network homeostasis.

2020-12-14 | GSE161540 | GEO

Oligodendrocyte-derived IL-33 functions as a microglial survival factor during neuroinvasive flavivirus infection

Project description:In order to recover from infection, organisms must balance robust immune responses to pathogens with the tolerance of immune-mediated pathology. This balance is particularly critical within the central nervous system, whose complex architecture, essential function, and limited capacity for self-renewal render it susceptible to both pathogen- and immune-mediated pathology. Here, we identify the alarmin IL-33 and its receptor ST2 as critical for host survival to neuroinvasive flavivirus infection. We identify oligodendrocytes as the critical source of IL-33, and microglia as the key cellular responders. Notably, we find that the IL-33/ST2 axis does not impact viral control or adaptive immune responses; rather, it is required to promote the activation and survival of microglia. In the absence of intact IL-33/ST2 signaling in the brain, neuroinvasive flavivirus infection triggered aberrant recruitment of monocyte-derived peripheral immune cells, increased neuronal stress, and neuronal cell death, effects that compromised organismal survival. These findings identify IL-33 as a critical mediator of CNS tolerance to pathogen-initiated immunity and inflammation.

2023-11-08 | GSE241804 | GEO

Astrocyte-derived Interleukin-33 promotes microglial synapse engulfment and neural circuit development II

Project description:Neuronal synapse formation and remodeling is essential to central nervous system (CNS) development and is dysfunctional in neurodevelopmental diseases. Innate immune signals regulate tissue remodeling in the periphery, but how this impacts CNS synapses is largely unknown. Here we show that the IL-1 family cytokine Interleukin-33 (IL-33) is produced by developing astrocytes and is developmentally required for normal synapse numbers and neural circuit function in the spinal cord and thalamus. We find that IL-33 signals primarily to microglia under physiologic conditions, that it promotes microglial synapse engulfment, and that it can drive microglial-dependent synapse depletion in vivo. These data reveal a cytokine-mediated mechanism required to maintain synapse homeostasis during CNS development.

2018-02-05 | GSE109353 | GEO

Astrocyte-derived Interleukin-33 promotes microglial synapse engulfment and neural circuit development I

2018-02-05 | GSE109352 | GEO

Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Determination of the molecular mechanism of IL33 on glioma cells Since IL-33 is known to associate with chromatin and regulate transcriptional activity and that nuclear expression of IL-33 increases glioma progression, we determined Nuclear IL-33 regulates the expression and secretion of inflammatory cytokines in glioma cells. Using these parameters 340 genes were induced by the ectopic expression of IL-33 and an additional 377 genes were downregulated. Gene ontology terms over-represented in the genes induced by IL-33 include three major clusters that associate with cytokine activity and inflammation

2020-08-21 | GSE153486 | GEO

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