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Gene expression data from S. aureus-exposed neutrophils

ABSTRACT: Neutrophil lysis after phagocytosis is a process potentially important in the pathogenesis of community-associated methicillin-resistant S. aureus (CA-MRSA) infection. The mechanism for this process is not currently known. Therefore, to better understand CA-MRSA virulence we used human oligonucleotide microarrays to investigate the mechanism underlying enhanced PMN lysis that occurs after phagocytosis of CA-MRSA. In order to examine the effect of S. aureus on the neutrophil transcriptome and to elucidate any possible differences in this effect between hospital- and community-associated S. aureus, we performed microarray expression analysis on human neutrophils treated with hospital- and community-associated S. aureus.

ORGANISM(S): Homo sapiens

PROVIDER: GSE16837 | GEO | 2010/06/01

SECONDARY ACCESSION(S): PRJNA117601

REPOSITORIES: GEO

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Transcription profiling of neutrophils exposed to S. aureus infection

Project description:Neutrophil lysis after phagocytosis is a process potentially important in the pathogenesis of community-associated methicillin-resistant S. aureus (CA-MRSA) infection. The mechanism for this process is not currently known. Therefore, to better understand CA-MRSA virulence we used human oligonucleotide microarrays to investigate the mechanism underlying enhanced PMN lysis that occurs after phagocytosis of CA-MRSA. In order to examine the effect of S. aureus on the neutrophil transcriptome and to elucidate any possible differences in this effect between hospital- and community-associated S. aureus, we performed microarray expression analysis on human neutrophils treated with hospital- and community-associated S. aureus. Polymorphonuclear leukocytes (PMNs) were isolated from the blood of healthy donors. Control and S. aureus-exposed PMNs were incubated at 37C for 1, 2, 3 or 6 hours.

2010-06-09 | E-GEOD-16837 | biostudies-arrayexpress

Prolonged intra-neutrophil survival as an adaptive strategy of Staphylococcus aureus USA300 to the hospital environment

Project description:Methicillin-resistant Staphylococcus aureus (MRSA) is the causative agent of serious hospital- and community-associated infections. Due to the global rise in community-associated MRSA, the respective lineages are increasingly introduced into hospitals. This raises the question whether and, if so, how they adapt to this new environment. The present study was aimed at investigating how MRSA isolates of the USA300 lineage, infamous for causing infections in the general population, have adapted to the hospital environment. To this end, a collection of community- and hospital-associated USA300 isolates was compared by RNA-sequencing. Here we report that merely 460 genes were differentially expressed between these two epidemiologically distinct groups, including genes for virulence factors, oxidative stress responses and the purine, pyrimidine and fatty acid biosynthetic pathways. Differentially regulated virulence factors included leukotoxins and phenol-soluble modulins, implicated in staphylococcal escape from immune cells. We therefore investigated the ability of the studied isolates to survive internalization by human neutrophils. This showed that the community-associated isolates have the highest neutrophil-killing activity, while the hospital-associated isolates are better adapted to intra-neutrophil survival. Importantly, the latter trait protects internalized staphylococci against a challenge with antibiotics. We therefore conclude that prolonged intra-neutrophil survival serves as a relatively simple early adaptation of S. aureus USA300 to the hospital environment where antibiotic pressure is high.

2016-11-02 | GSE89394 | GEO

Next generation sequencing allows identification of quantitave differential gene expression between four clinical strains of methicilin resistant Staphylococcus aureus

Project description:Staphylococcus aureus can cause a broad spectrum of diseases that vary widely in clinical presentation and disease severity[121]. Methicillin-Resistant S. aureus (MRSA) strains first described in the 1960’s[122] were hospital acquired (HA MRSA), however in the 1990’s, community-associated MRSA strains (CA MRSA) were identified and are considered to be more virulent[16]. Therapeutics and management of MRSA focuses on novel antibacterials and vaccines targeting virulence factors. To date no clinical trials for vaccines have succeeded[123] due to the poor understanding of the pathogenic mechanisms exhibited by S.aureus.We investigated the differential gene expression of four clinical MRSA strains in vitro, belonging to HA and CA MRSA, at the stationary and exponential growth phases, using RNA-seq on the Ion torrent next generation sequencing platform. This study reveals the high diversity of virulence trait expression among MRSA strains within strains as well as between different growth phases, and also suggests potential factors other than PVL that contributes to enhanced virulence in CA MRSA

2020-01-07 | GSE70636 | GEO

The SaeR/S Gene Regulatory System is Essential for Innate Immune Evasion by Staphylococcus aureus

Project description:Methicillin-resistant Staphylococcus aureus (MRSA) is problematic both in hospitals and the community. Currently, we have limited understanding of mechanisms of innate immune evasion used by S. aureus. To that end, we created an isogenic deletion mutant in strain MW2 (USA400) of the saeR/S two-component gene regulatory system and studied its role in mouse models of pathogenesis and during human neutrophil interaction. In this study, we demonstrate saeR/S plays a distinct role in S. aureus pathogenesis and is vital for virulence of MW2 in a mouse model of sepsis. Moreover, deletion of saeR/S significantly impaired survival of MW2 in human blood and after neutrophil phagocytosis. Microarray analysis of genes influenced by saeR/S demonstrated SaeR/S of MW2 influences a wide variety of genes with diverse biological functions. These data shed new insight into how virulence is regulated in S. aureus and associates a specific staphylococcal gene-regulatory system with invasive staphylococcal disease. Wild type control vs mutant at two different growth phases

2010-05-14 | E-GEOD-15067 | biostudies-arrayexpress

Panton-Valentine Leukocidin Does Not Impact Virulence of Community-associated MRSA

Project description:Panton-valentine leukocidin (PVL) has been linked to worldwide emergence of community-associated methicillin resistant Staphylococcus aureus (CA-MRSA) -- its role in virulence in unclear. Here we show that PVL had no effect on global gene expression of prominent CA-MRSA strains nor did it affect bacterial clearance from lungs, spleen and kidneys in a highly discriminatory rabbit bacteremia model. These findings negate a large body of epidemiological research that implicated PVL in CA-MRSA virulence. Keywords: mutant vs wild type in 2 different growth phases grown in 2 different medias

2008-09-12 | GSE8677 | GEO

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Project description:The epidemic community-acquired methicillin-resistant S. aureus (CA-MRSA) clone USA300 has recently become a leading cause of hospital-associated bloodstream infections (BSI). Leveraging this recent introduction into hospitals and the limited genetic variation across the USA300 strains, we combined microbial comparative genomics with phenotypic analyses to discover adaptive mutations. USA300 isolates from BSI were found to have independently evolved single nucleotide variants in the transcriptional regulator sarZ. sarZ inactivation lead to altered expression of virulence factors, resulting in increased lethality in a murine model of BSI. Thus, USA300 strains can optimize their fitness in hospitals through evolution of higher virulence.

2022-10-08 | GSE185544 | GEO

Role of the accessory gene regulator agr in community-associated MRSA pathogenesis

Project description:The success of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) as pathogens is due to a combination of antibiotic resistance with high virulence. However, evolution of the exceptional virulence potential of CA-MRSA is not understood. Our previous study indicated that differential gene expression contributes substantially to this process. Thus, we here investigated the role of the pivotal virulence gene regulatory system agr in the most prevalent CA-MRSA strain USA300. Using a mouse subcutaneous infection model, we show that agr is essential for the development of CA-MRSA skin infections, the most frequent manifestation of disease caused by CA-MRSA. Furthermore, genome-wide analysis of gene expression revealed significant differences in agr-dependent virulence gene regulation between CA-MRSA, HA-MRSA, and laboratory strains. Our findings demonstrate that agr functionality is critical for CA-MRSA disease and indicate that an adaptation of the agr regulon to optimize expression of a broad set of virulence determinants may have contributed to the evolution of exceptionally pronounced virulence of CA-MRSA strains. Keywords: wild type vs mutant

2011-03-29 | GSE18793 | GEO

The SaeR/S Gene Regulatory System is Essential for Innate Immune Evasion by Staphylococcus aureus

2010-02-23 | GSE15067 | GEO

TSLP acts on neutrophils to drive complement-mediated killing of methicillin-resistant Staphylococcus aureus

Project description:Staphylococcus aureus can cause serious skin, respiratory, and other life-threatening invasive infections in humans, and methicillin-resistant S. aureus (MRSA) strains have been acquiring increasing antibiotic resistance. While MRSA was once mainly considered a hospital-acquired infection, the emergence of new strains, some of which are pandemic, has resulted in community-acquired MRSA infections that often present as serious skin infections in otherwise healthy individuals. Accordingly, defining the mechanisms that govern the activation and regulation of the immune response to MRSA is clinically important and could lead to the discovery of much needed rational targets for therapeutic intervention. Because the cytokine thymic stromal lymphopoetin (TSLP) is highly expressed by keratinocytes of the skin3, we investigated its role in host-defense against MRSA. Here we demonstrate that TSLP acts on neutrophils to increase their killing of MRSA. In particular, we show that both mouse and human neutrophils express functional TSLP receptors. Strikingly, TSLP enhances mouse neutrophil killing of MRSA in both an in vitro whole blood killing assay and an in vivo skin infection model. Similarly, TSLP acts directly on purified human blood neutrophils to reduce MRSA burden. Unexpectedly, we demonstrate that TSLP mediates these effects both in vivo and in vitro by engaging the complement C5 system. Thus, TSLP increases MRSA killing in a neutrophil- and complement-dependent manner, revealing a key connection between TSLP and the innate complement system, with potentially important therapeutic implications for control of MRSA infection.

2016-11-18 | GSE73313 | GEO

RNA-seq of Wildtype Staphylococcus aureus USA300 NRS384

Project description:Methicillin-resistant Staphylococcus aureus (MRSA) infections result in more than 200,000 hospitalizations and 10,000 deaths in the United States each year and remain an important medical challenge. To better understand the transcriptome of Staphylococcus aureus USA300 NRS384, a community-acquired MRSA strain, we have conducted an RNA-Seq experiment on WT samples.

2017-11-15 | GSE102279 | GEO

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