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Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection

ABSTRACT: Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection

PROVIDER: PRJNA731042 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14585338_1.fastq.gz	Fastqsanger.gz
	SRR14585338_2.fastq.gz	Fastqsanger.gz
	SRR14585339_1.fastq.gz	Fastqsanger.gz
	SRR14585339_2.fastq.gz	Fastqsanger.gz
	SRR14585340_1.fastq.gz	Fastqsanger.gz

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Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 1]

Project description:Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 1]

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Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 2]

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Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 2]

Project description:Dermal macrophages (Macs) are essential for the timely resolution of staphylococcal skin infections. However the cell intrinsic pathways and microenvironmental cues that mediate this are unclear. Here we analyzed a strictly intradermal ear infection model with Staphylococcus aureus (S. aureus) to explore immunometabolic regulation.

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Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 1]

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

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Different pathogenic stimuli induce specific metabolic rewiring in human monocytes

Project description:Recent studies have demonstrated that upon encountering a pathogenic stimulus, robust metabolic rewiring of immune cells occurs. A switch away from oxidative phosphorylation to glycolysis, even in the presence of sufficient amounts of oxygen (akin the Warburg effect), is typically observed in activated innate and adaptive immune cells and is thought to accommodate adequate inflammatory responses. However, whether the Warburg effect is a general phenomenon applicable in human monocytes exposed to different pathogenic stimuli is unknown. Our results using human monocytes from healthy donors demonstrate that the Warburg effect only holds true for TLR4 activated cells. Although activation of other TLRs leads to an increase in glycolysis, no reduction or even an enhancement in oxidative phosphorylation is observed. Moreover, specific metabolic rewiring occurs in TLR4 vs. TLR2 stimulated cells characterized by altered gene expression profiles of pathways related to metabolism, changes in spare respiratory capacity of the cells and differential regulation of mitochondrial enzyme activity. Similarly, results from ex vivo and in vivo studies demonstrate metabolic rewiring of immune cells that is highly dependent on the type of pathogenic stimulus. Although the Warburg effect is observed in human monocytes after TLR4 activation, we propose that this typical metabolic response is not applicable to other inflammatory signalling routes including TLR2 in human monocytes. Instead, each pathogenic stimulus and subsequently activated inflammatory signalling cascade induces specific metabolic rewiring of the immune cell to accommodate an appropriate response.

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