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Noncanonical Il-1β maturation in microglia impairs cognition in chronic kidney disease via neuronal IL1R signaling

ABSTRACT: Noncanonical Il-1β maturation in microglia impairs cognition in chronic kidney disease via neuronal IL1R signaling

PROVIDER: PRJNA904656 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22388700_1.fastq.gz	Fastqsanger.gz
	SRR22388700_2.fastq.gz	Fastqsanger.gz
	SRR22388701_1.fastq.gz	Fastqsanger.gz
	SRR22388701_2.fastq.gz	Fastqsanger.gz
	SRR22388702_1.fastq.gz	Fastqsanger.gz

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Noncanonical Il-1β maturation in microglia impairs cognition in chronic kidney disease via neuronal IL1R signaling

Project description:While cognitive impairment is common in peripheral diseases such as chronic kidney disease (CKD), mechanistic insights and effective therapies are lacking. Here, we show that microglial potassium (K+) dyshomeostasis induces noncanonical IL-1β maturation and neuronal dysfunction via IL-1R signaling in CKD. Despite inflammasome activation in the brain, microglial caspase-1 deficiency does not improve inflammation and cognition in CKD mice. Noncanonical IL-1β maturation in microglia is mediated by the cathepsin C–caspase-8 pathway. Restoring K+ homeostasis in microglia or genetically inhibiting neuronal IL-1R1 signaling abolishes CKD-induced cognitive impairment. Microglial K+ dyshomeostasis and noncanonical microglial IL-1β maturation may therefore be druggable targets in some forms of cognitive impairment. These insights identify a new intercellular microglia–neuron crosstalk and identify potential therapeutic targets to combat inflammasome-induced neuronal dysfunction.

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