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Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (glycerol or succinate)

ABSTRACT: Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (glycerol or succinate)

PROVIDER: PRJNA578747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10320667_1.fastq.gz	Fastqsanger.gz
	SRR10320667_2.fastq.gz	Fastqsanger.gz
	SRR10320668_1.fastq.gz	Fastqsanger.gz
	SRR10320668_2.fastq.gz	Fastqsanger.gz
	SRR10320669_1.fastq.gz	Fastqsanger.gz

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Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (glycerol or succinate)

Project description:Intracellular pathogens, such as Salmonella enterica serovar Typhimurium (S.Tm), are able to sense and respond to a changing host cell environment. Macrophages exposed to microbial products undergo metabolic changes that are increasingly understood to drive a productive inflammatory response. However, the role of macrophage metabolic reprogramming in bacterial adaptation to the intracellular environment has not been explored. Here we show that changes in host metabolic state serve as a signal detected byS.Tm. Using metabolic profiling and dual RNA-seq, we show that succinate accumulates in infected macrophages and is sensed by intracellular S.Tm to promote induction of virulence genes. Succinate uptake by the bacterium drives induction of pmrAB-dependent genes and SPI-2 virulence-associated regulon. S.Tm lacking the DcuB transporter for succinate uptake display impaired intracellular survival. Our work demonstrates that accumulation of metabolic intermediates, necessary for macrophage activation, promote intracellular survival of pathogens, opening a new realm of metabolic host-pathogen crosstalk.

2022-10-19 | GSE139207 | GEO

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (host and bacteria)

2022-10-19 | GSE139205 | GEO

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (2DG)

2022-10-19 | GSE139206 | GEO

Catabolite repression by intracellular succinate in Campylobacter jejuni

Project description:Catabolite repression by intracellular succinate in Campylobacter jejuni

| PRJNA412095 | ENA

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (2DG)

Project description:Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (2DG)

| PRJNA578745 | ENA

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (host and bacteria)

Project description:Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (host and bacteria)

| PRJNA578744 | ENA

Catabolite repression by intracellular succinate in Campylobacter jejuni

Project description:Bacteria have evolved different mechanisms to catabolize carbon sources from a mixture of nutrients. They first consume their preferred carbon source, before others are used. Regulatory mechanisms adapt the metabolism accordingly to maximize growth and to outcompete other organisms. The human pathogen Campylobacter jejuni is an asaccharolytic Gram-negative bacterium that catabolizes amino acids and organic acids for growth. It prefers serine and aspartate as carbon sources, however it lacks all regulators known to be involved in regulating carbon source utilization in other organisms. In which manner C. jejuni adapts its metabolism towards the presence or absence of preferred carbon sources is unknown. In this study, we show with transcriptomic analysis and enzyme assays how C. jejuni adapts its metabolism in response to its preferred carbon source serine. In the presence of serine as well as lactate and pyruvate C. jejuni represses the utilization of other carbon sources, by repressing the expression of a number of central metabolic enzymes. The regulatory proteins RacR, Cj1000 and CsrA play a role in the regulation of these metabolic enzymes. This metabolism dependent transcriptional repression correlates with an accumulation of intracellular succinate. Hence, we propose a demand-based catabolite repression mechanism in C. jejuni, which depends on the intracellular succinate level.

2017-10-01 | GSE104231 | GEO

Host succinate is a signal for activation of Salmonella virulence during intracellular infection

Project description:Host succinate is a signal for activation of Salmonella virulence during intracellular infection

| PRJNA578741 | ENA

Gene expression for Escherichia coli BW25113 exponential growth on minimal medium with eight different carbon sources: Glucose, Galactose, Glycerol, Gluconate, Fructose, Pyruvate, Succinate, Acetate.

Project description:This dataset contains the gene expression signature in triplicates of Escherichia coli BW25113 growing exponentially on eight different environments: minimal medium supplemented with 5 g/L of Glucose, Galactose, Glycerol, Gluconate, Fructose, Pyruvate, Succinate or Acetate as the sole carbon source.

2015-10-07 | E-MTAB-3392 | biostudies-arrayexpress

Nutritional immunity promotes intracellular survival of nontypeable Haemophilus influenzae

Project description:Nutritional immunity promotes intracellular survival of nontypeable Haemophilus influenzae via altered intracellular trafficking

2018-05-24 | MSV000082399 | MassIVE

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