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

ABSTRACT: 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.

ORGANISM(S): Sus scrofa

PROVIDER: GSE201550 | GEO | 2022/06/29

REPOSITORIES: GEO

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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

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

| PRJNA832210 | ENA

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

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 preterm newborns infected with Staphylococcus epidermidis [whole blood]

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

| PRJNA832220 | ENA

Toxin mediates sepsis caused by methicillin-resistant Staphylococcus epidermidis

Project description:Bacterial sepsis is a major killer in hospitalized patients. Coagulase-negative staphylococci (CNS) with the leading species Staphylococcus epidermidis are the most frequent causes of nosocomial sepsis, with most infectious isolates being methicillin resistant. However, which bacterial factors underlie the pathogenesis of CNS sepsis is unknown. While it has been commonly believed that invariant structures on the surface of CNS trigger sepsis by causing an over-reaction of the immune system, we show here that sepsis caused my methicillin-resistant S. epidermidis is to a large extent mediated by the methicillin resistance island-encoded peptide toxin, PSM-mec. PSM-mec contributed to bacterial survival in whole human blood and resistance to neutrophil-mediated killing, and caused significantly increased mortality and cytokine expression in a mouse sepsis model. Furthermore, we show that the PSM-mec peptide itself, rather than the regulatory RNA in which its gene is embedded, is responsible for the observed virulence phenotype. While toxins have never been clearly indicated in CNS infections, our study shows that an important type of infection caused by the predominant CNS species, S. epidermidis, is mediated to a large extent by a toxin. Of note, these findings suggest that CNS infections may be amenable to virulence-targeted drug development approaches. We used microarrays to detail the global gene expression between S. epidermidis strain Rp62A and S. epidermidis strain Rp62A isogenic Δpsm-mec deletion mutants

2017-01-06 | GSE85265 | GEO

Citrulline supplementation leads to increased immune suppression and more severe outcomes in infected newborn piglets

Project description:Background: Preterm infants are at high risk of infection and sepsis, which is associated with arginine (ARG) deficiency. Optimal nutrition for preterm newborns suspected with infection is critical to prevent sepsis development. Citrulline (CIT) supplementation is known to prevent sepsis in adult rodents, by maintaining sufficient blood ARG levels and vascular stabilization. We hypothesized that CIT therapy improve sepsis outcomes in infected preterm newborns via CIT and ARG metabolism.Results: After infection, oral CIT supplementation led to higher mortality, blood bacterial load, and circulating and hepatic inflammation, compared with the infected controls. Intravenous CIT administration also showed increased inflammation and bacterial burdens without increased mortality. Liver transcriptomics and data from in vitro blood stimulation indicated that CIT induces enhanced immunosuppression, which may impair resistance response to bacteria at early stage of infection and later cause excessive inflammation and tissue damage. Conclusion: Early stage of CIT supplementation exacerbates sepsis severity in infected preterm pigs, likely via induced enhanced systemic immunosuppression.

2023-11-20 | GSE247865 | GEO

AI-2-dependent gene regulation in Staphylococcus epidermidis

Project description:Autoinducer 2 (AI-2), a widespread by-product of the LuxS-catalyzed S-ribosylhomocysteine cleavage reaction in the activated methyl cycle, has been suggested to serve as an intra- and interspecies signaling molecule, but in many bacteria AI-2 control of gene expression is not completely understood. Particularly, we have a lack of knowledge about AI-2 signaling in the important human pathogens Staphylococcus aureus and S. epidermidis. Here, to determine the role of LuxS and AI-2 in S. epidermidis, we analyzed genome-wide changes in gene expression in an S. epidermidis luxS mutant and after addition of AI-2 synthesized by over-expressed S. epidermidis Pfs and LuxS enzymes. Genes under AI-2 control included mostly genes involved in sugar, nucleotide, amino acid, and nitrogen metabolism, but also virulence-associated genes coding for lipase and bacterial apoptosis proteins. In addition, we demonstrate by liquid chromatography/mass-spectrometry of culture filtrates that the pro-inflammatory phenol-soluble modulin (PSM) peptides, key virulence factors of S. epidermidis, are under luxS/AI-2 control. Our results provide a detailed molecular basis for the role of LuxS in S. epidermidis virulence and suggest a signaling function for AI-2 in this bacterium. Keywords: wild type without glucose control vs luxS mutant vs luxS mutant with auto-inducer II wild type without glucose control vs luxS mutant vs luxS mutant with auto-inducer II

2008-10-10 | E-GEOD-9427 | biostudies-arrayexpress

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