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E-GEOD-44943

ABSTRACT: HIF-1 dependent gene expression upon S. aureus infection

OTHER RELATED OMICS DATASETS IN: PRJNA192586

PROVIDER: E-GEOD-44943 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-44943-analysis-methods.tsv	Tabular
	E-GEOD-44943-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-44943-configuration.xml	Xml
	E-GEOD-44943-percentile-ranks.tsv	Tabular
	E-GEOD-44943.condensed-sdrf.tsv	Tabular

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Project description:HIF-1 dependent gene expression upon S. aureus infection

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HIF-1 dependent gene expression upon S. aureus infection

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HIF-1 dependent gene expression upon S. aureus infection

Project description:HIF-1 is an important transcription factor for immune responses to bacterial infection. We wanted to analyze the HIF-1 dependent gene expression upon S. aureus infection and analyzed the gene expression of HepG2 nt and HepG2 HIF-1-/- cells four hours upon infection using affymetrix human gene 1.0 st. gene arrays. triplicates of HepG2 nt and HepG2 HIF-1-/- cells were infected with S. aureus 8325-4 (4 h, MOI: 20), triplicates of uninfected cells were used as control

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Project description:IκBζ-dependent responses in keratinocytes upon Staphylococcus aureus infection

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Gene expression profiles of ears infected with Staphylococcus aureus at ZT4

Project description:We analysed the gene expression profiles after infection of Staphylococcus aureus at ZT4 in CXCL14-KO mice. The group of genes categolized as GO defense response (GO: 006952) were upregulated upon a response to Staphylococcus aureus infection. The expression of IL1b, Cxcl2, and Ccl3 were significantly suppressed in infected ear of Cxcl14-KO compared to that of WT.

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Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils. Lesional skin biopsies obtained from C57BL/6J WT mice or IL-1R-deficient mice at 4 hours post-infection with Staphylococcus aureus. Uninfected skin biopsies were also collected from WT and IL-1R-deficient mice.

2012-12-05 | E-GEOD-36826 | biostudies-arrayexpress

Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

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Gene Expression-Based Classifiers Identify Staphylococcus aureus Infection in Mice and Humans

Project description:Staphylococcus aureus causes a spectrum of human infection. Diagnostic delays and uncertainty lead to treatment delays and inappropriate antibiotic use. A growing literature suggests the host’s inflammatory response to the pathogen represents a potential tool to improve upon current diagnostics. The hypothesis of this study is that the host responds differently to S. aureus than to E. coli infection in a quantifiable way, providing a new diagnostic avenue. This study uses Bayesian sparse factor modeling and penalized binary regression to define peripheral blood gene-expression classifiers of murine and human S. aureus infection. The murine-derived classifier distinguished S. aureus infection from healthy controls and Escherichia coli-infected mice across a range of conditions (mouse and bacterial strain, time post infection) and was validated in outbred mice (AUC>0.97). A S. aureus classifier derived from a cohort of 95 human subjects distinguished S. aureus blood stream infection (BSI) from healthy subjects (AUC 0.99) and E. coli BSI (AUC 0.82). Murine and human responses to S. aureus infection share common biological pathways, allowing the murine model to classify S. aureus BSI in humans (AUC 0.84). Both murine and human S. aureus classifiers were validated in an independent human cohort (AUC 0.95 and 0.94, respectively). The approach described here lends insight into the conserved and disparate pathways utilized by mice and humans in response to these infections. Furthermore, this study advances our understanding of S. aureus infection; the host response to it; and identifies new diagnostic and therapeutic avenues.

2013-01-11 | GSE33341 | GEO

IκBζ-dependent responses in keratinocytes upon Staphylococcus aureus infection

Project description:In this study we investigated the transcriptional responses of keratinocyte-derived IκBζ (encoded by NFKBIZ) upon infection with the pathogenic Staphylococcus aureus (S. aureus) USA300 wildtype strain.

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Project description:Staphylococcus aureus is a significant cause of human infection. Here, we demonstrate that mutations in the transcriptional repressor of purine biosynthesis, purR, enhance the pathogenic potential of S. aureus. Indeed, systemic infection with purR mutants causes accelerated mortality in mice, which is due to aberrant up-regulation of fibronectin binding proteins (FnBPs). Remarkably, purR mutations can arise upon exposure of S. aureus to stress, such as an intact immune system. In humans, naturally occurring anti-FnBP antibodies exist that, while not protective against recurrent S. aureus infection, ostensibly protect against hypervirulent S. aureus infections. Vaccination studies support this notion, where anti-Fnb antibodies in mice protect against purR hypervirulence. These findings provide a novel link between purine metabolism and virulence in S. aureus.

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