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Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [whole blood]

ABSTRACT: Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [whole blood]

PROVIDER: PRJNA832220 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18923152_1.fastq.gz	Fastqsanger.gz
	SRR18923152_2.fastq.gz	Fastqsanger.gz
	SRR18923153_1.fastq.gz	Fastqsanger.gz
	SRR18923153_2.fastq.gz	Fastqsanger.gz
	SRR18923154_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [whole blood]

Project description:To investigate if appropriately adjusted parenteral glucose supply and/or temporary glycolysis inhibition by administration may help to prevent sepsis or improve sepsis outcomes of preterm newborns, we using a preterm pig model inoculated with Staphylococcus epidermidis to mimic the inflammation condition of preterm newborns at birth and treated them with different parenteral nutrition glucose supplyment and glycolysis inhibitor administration. We then performed gene expression profiling analysis using data obtained from RNA-seq of preterm pigs` whole blood, which collected at 12 hours after SE infection, treated with different parenteral glucose supply and glycolysis inhibitor administration.

2022-06-29 | GSE201552 | GEO

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [cord blood]

Project description:To investigate the glycolysis inhibition effect on the inflammation responses of preterm newborns infected with Staphylococcus epidermidis, we used preterm pigs` cord blood to mimic the inflammation condition of preterm newborns at birth and stimulated with S. epidermidis and glycolysis inhibior. We then performed gene expression profiling analysis using data obtained from RNA-seq of the cord blood, which were stimulated with S. epidermidis and DCA.

2022-06-29 | GSE201539 | GEO

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [liver]

Project description:To investigate if appropriately adjusted parenteral glucose supply may help to shift liver metabolism profiling to further prevent sepsis or improve sepsis outcomes of preterm newborns, we using a preterm pig model inoculated with Staphylococcus epidermidis to mimic the inflammation condition of preterm newborns at birth and treated them with different parenteral nutrition glucose supplyment. We then performed gene expression profiling analysis using data obtained from RNA-seq of preterm pigs` liver tissue, which collected at 22 hours after SE infection, treated with different parenteral glucose supply.

2022-06-29 | GSE201550 | GEO

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis

Project description:Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis

| PRJNA832210 | ENA

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [liver]

Project description:Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [liver]

| PRJNA832221 | ENA

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [cord blood]

Project description:Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [cord blood]

| PRJNA832151 | ENA

Glucose supply and glycolysis inhibition shape the clinical fate of Staphylococcus epidermidis-infected preterm newborns.

Project description:Preterm infants are susceptible to bloodstream infection by coagulase-negative staphylococci (CONS) that can lead to sepsis. Glucose-rich parenteral nutrition is commonly used to support the infants' growth and energy expenditure but may exceed endogenous regulation during infection, causing dysregulated immune response and clinical deterioration. Using a preterm piglet model of neonatal CONS sepsis induced by Staphylococcus epidermidis (S. epidermidis) infection, we demonstrate the delicate interplay between immunity and glucose metabolism to regulate the host infection response. Circulating glucose levels, glycolysis, and inflammatory response to infection are closely connected across the states of tolerance, resistance, and immunoparalysis. Furthermore, high parenteral glucose provision during infection induces hyperglycemia, elevated glycolysis, and inflammation, leading to metabolic acidosis and sepsis, whereas glucose-restricted individuals are clinically unaffected with increased gluconeogenesis to maintain moderate hypoglycemia. Finally, standard glucose supply maintaining normoglycemia or pharmacological glycolysis inhibition enhances bacterial clearance and dampens inflammation but fails to prevent sepsis. Our results uncover how blood glucose and glycolysis control circulating immune responses, in turn determining the clinical fate of preterm infants infected with CONS. Our findings suggest further refinements of the current practice of parenteral glucose supply for preterm infants during infection.

| S-EPMC9220920 | biostudies-literature

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis

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

2022-06-29 | GSE201554 | GEO

Proteomics identifies lipocalin 2 in neonatal inflammation associated with cerebrovascular alteration in mice and preterm infants

Project description:Staphylococcus (S.) epidermidis is one of the most common nosocomial coagulase-negative staphylococci infections in preterm infants. The clinical signs of infection are often unspecific and identification of novel markers to complement the current diagnosis is needed. In this study, we investigated proteomic alterations in the neonatal mouse brain following S. epidermidis infection and in the blood in preterm infants. We identified lipocalin 2 (LCN2) as a crucial protein associated with cerebrovascular changes and astrocyte reactivity in mice. While astrocytes were activated in S. epidermidis infected mice, LCN2 protein expression in the brain was associated with endothelial cells but not astrocyte reactivity. By combining weighted gene co-expression analysis and differential expression approaches, we further identified that LCN2 protein was linked to blood C-reactive protein levels in a cohort of preterm infants born <28 weeks of gestation. Blood LCN2 levels were associated with similar alterations of cytokines and chemokines in both infected mice and human preterm infants with increased levels of CRP. The present experimental and clinical study indicates that LCN2 might be a suitable additional marker of preterm infection/inflammation associated with cerebrovascular changes and neuroinflammation.

2023-10-24 | PXD041926 | Pride

RNA-sequencing of neonatal monocyte responses to E. coli and S. epidermidis

Project description:Newborns, particularly those born prematurely, are extremely vulnerable to sepsis and this has been attributed to ‘immature’ innate monocyte defences. Predominant pathogens include Escherichia. coli and Staphylococcus. epidermidis but no studies have assessed global transcriptional responses of neonatal monocytes to live sepsis-causing bacteria. Here, we aimed to identify and characterise the common and pathogen-specific, neonatal monocyte transcriptional responses to E. coli and S. epidermidis to better understand early life innate immune responses. RNA-sequencing was performed on purified cord blood monocytes from very preterm (<32 weeks gestational age, GA) and term infants (37-40 weeks GA) following standardised challenge with live S. epidermidis or E. coli.

2018-03-16 | GSE101880 | GEO

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