Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of S. epidermidis phenol-soluble modulins on primary human keratinocytes.

ABSTRACT: To investigate the effect of synthetic phenol-soluble modulins (PSMs) secreted by S. epidermidis on primary keratinocytes. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

ORGANISM(S): Homo sapiens

PROVIDER: GSE209653 | GEO | 2023/01/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of S. epidermidis phenol-soluble modulins on murine dorsal skin (24h)

Project description:To investigate the effect of both S. epidermidis phenol-soluble modulins (PSMs) and EcpA genetic knockouts on murine back skin. We then performed gene expression profiling analysis using data obtained from RNA-seq of 5 conditions (n=3 per condition).

2023-07-01 | GSE210046 | GEO

Effect of S. epidermidis phenol-soluble modulins on primary human keratinocytes.

Project description:Effect of S. epidermidis phenol-soluble modulins on primary human keratinocytes.

| PRJNA861992 | ENA

Effect of S. epidermidis phenol-soluble modulins on murine dorsal skin (24h)

Project description:Effect of S. epidermidis phenol-soluble modulins on murine dorsal skin (24h)

| PRJNA863579 | ENA

RNA-Seq analysis of human keratinocytes stimulated with synthetic PSMα3

Project description:To determine the genes that change mRNA transcript abundance in primary human keratinocytes treated by S. aureus phenol-soluble modulins (PSM), we stimulated keratinocytes for 24h with either DMSO(-) Ctl or synthetic PSMα3 (5μg/mL).

2019-03-05 | GSE124818 | 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

AI-2-dependent gene regulation in Staphylococcus epidermidis

2008-10-10 | GSE9427 | GEO

The small RNA Teg41 Regulates Expression of the alpha Phenol Soluble Modulins and is Required for Virulence in Staphylococcus aureus

Project description:The small RNA Teg41 Regulates Expression of the alpha Phenol Soluble Modulins and is Required for Virulence in Staphylococcus aureus

| PRJNA423193 | ENA

Rapid pathogen-specific recruitment of immune effector cells in the skin by secreted toxins

Project description:Swift recruitment of phagocytic leukocytes is critical to prevent infection when bacteria breach through the protective layers of the skin. According to canonical models, this occurs via an indirect process that is initiated by contact of bacteria with resident skin cells and which is independent of the pathogenic potential of the invader. Here, we describe a more rapid mechanism of leukocyte recruitment to the site of intrusion of the important skin pathogen Staphylococcus aureus that is based on direct recognition of specific bacterial toxins, the phenol-soluble modulins (PSMs), by circulating leukocytes. This early recruitment was dependent on the transcription factor EGR1 and significantly contributed to the prevention of infection. Our findings refine the classical notion of the non-specific and resident cell-dependent character of the innate immune response to bacterial infection by demonstrating a pathogen-specific high-alert mechanism involving direct recruitment of immune effector cells by secreted bacterial products.

2021-10-25 | GSE103779 | GEO

The stringent response of Staphylococcus aureus and its impact on survival after phagocytosis through the induction of intracellular PSMs expression

Project description:The stringent response is initiated by rapid (p)ppGpp synthesis, which leads to a profound reprogramming of gene expression in most bacteria. The stringent phenotype seems to be species specific and may be mediated by fundamentally different molecular mechanisms. In Staphylococcus aureus, (p)ppGpp synthesis upon amino acid deprivation is achieved through the synthase domain of the bifunctional enzyme RSH (RelA/SpoT homolog). In several firmicutes, a direct link between stringent response and the CodY regulon was proposed. Wild-type strain HG001, rshSyn, codY and rshSyn, codY double mutants were analyzed by transcriptome analysis to delineate different consequences of RSH-dependent (p)ppGpp synthesis after induction of the stringent response by amino-acid deprivation. Under these conditions genes coding for major components of the protein synthesis machinery and nucleotide metabolism were down-regulated only in rsh positive strains. Genes which became activated upon (p)ppGpp induction are mostly regulated indirectly via de-repression of the GTP-responsive repressor CodY. Only seven genes, including those coding for the cytotoxic phenol-soluble modulins (PSMs), were found to be up-regulated via RSH independently of CodY. qtRT-PCR analyses of hallmark genes of the stringent response indicate that an RSH activating stringent condition is induced after uptake of S. aureus in human polymorphonuclear neutrophils (PMNs). The RSH activity in turn is crucial for intracellular expression of psms. Accordingly, rshSyn and rshSyn, codY mutants were less able to survive after phagocytosis similar to psm mutants. Intraphagosomal induction of psma1-4 and/or psmM-CM-^_1,2 could complement the survival of the rshSyn mutant. Thus, an active RSH synthase is required for intracellular psm expression which contributes to survival after phagocytosis. Microarray was used to evaluate alteration in the transcriptome of codY and rsh mutants and compared to the wild type

2013-04-05 | E-GEOD-45617 | biostudies-arrayexpress

Expression of candidate genes by keratinocytes co-cultured with skin commensal

Project description:To investigate whether skin bacteria might influence the expression of selected genes, we co-cultured human keratinocytes with S. epidermidis, an abundant commensal in human skin and performed RNA sequencing analysis.

2021-11-11 | GSE188576 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data