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IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia

ABSTRACT: IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia

PROVIDER: PRJNA1190424 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31502621.fastq.gz	Fastqsanger.gz
	SRR31502622.fastq.gz	Fastqsanger.gz
	SRR31502623.fastq.gz	Fastqsanger.gz
	SRR31502624.fastq.gz	Fastqsanger.gz
	SRR31502625.fastq.gz	Fastqsanger.gz

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IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia [snRNA-Seq]

Project description:Invasive C. albicans infections result in high mortality rates. While IL-1 is important to combat these infections, the precise mode of action remains unclear. Using global and conditional Il1r1 knockouts in mice, we found that IL-1R-signaling in non-hematopoietic cells in the kidney and brain is crucial for a protective response. In the kidney, endothelial IL-1R contributes to fungal clearance independent of neutrophil recruitment, while IL-1R in hematopoietic cells is dispensable. In the brain, IL-1R-signaling indirectly recruits neutrophils and monocytes by regulating chemokines and adhesion molecules. Single-nucleus-RNA-sequencing revealed Il1r1-mediated NF-B-activation in distinct kidney cell types. Our data reveal excessive metabolic activity and oxidative phosphorylation across all cell types in the kidney of Il1r1-deficient mice within a few hours upon infection, associated with localized hypoxia at infection foci. By showing that hypoxia promotes fungal growth and pathogenicity, our data suggest that IL-1R-signaling in non-hematopoietic cells is required to prevent fatal candidiasis by inhibiting a metabolic shift, including excessive oxidative phosphorylation and hypoxia.

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Project description:The opportunistic fungal pathogen Candida albicans is a common cause of life-threatening nosocomial bloodstream infections. In the murine model of systemic candidiasis the kidney is the primary target organ while the fungal load declines over time in liver and spleen. To get a better understanding of the organ-specific differences in host-pathogen interaction during systemic murine candidiasis, we performed a time-course gene expression profiling to investigate the differential responses of murine kidney, liver and spleen and determined the fungal transcriptome in liver and kidney. We clearly demonstrate a delayed immune response on the transcriptional level in kidney accompanied by late induction of fungal stress response genes in this organ. In contrast, early upregulation of the proinflammatory response in the liver was associated with a fungal transcriptional profile resembling that of phagocytosed cells, suggesting that the resident phagocytic system contributes significantly to fungal control in the liver. Although no visible filamentation occurred in the liver, C. albicans hypha-associated genes were upregulated, indicating an uncoupling of gene expression and morphology during infection of this organ. In vitro the induction of hypha-associated gene expression in yeast cells led to altered interaction with macrophages, suggesting that the observed transcriptional changes affect host-pathogen interaction in vivo. Consistently, the combination of host and pathogen transcriptional data in an inference network model implied that C. albicans cell wall remodeling and metabolism were connected to the immune responses in kidney and liver. Furthermore, the network suggested links between fungal iron acquisition and amino acid metabolism in the kidney and host organ homeostasis. Thus, this work provides novel insights into the organ-specific host-pathogen interactions during systemic C. albicans infection.

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