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Homo sapiens

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

PROVIDER: PRJNA296577 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2480490.fastq.gz	Fastqsanger.gz
	SRR2480500.fastq.gz	Fastqsanger.gz
	SRR2480491.fastq.gz	Fastqsanger.gz
	SRR2480492.fastq.gz	Fastqsanger.gz
	SRR2480493.fastq.gz	Fastqsanger.gz

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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.

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Potential Mechanism of Action of 3'-Demethoxy-6-O-Demethylisoguaiacin on Methicillin-resistant Staphylococcus aureus

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Project description:The Impact of CodY on Virulence Determinant Production in Community-Associated Methicillin Resistant Staphylococcus aureus

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Further Insights into the Mode of Action of the Lipoglycopeptide Telavancin through Global Gene Expression Studies

Project description:Background: Telavancin is a novel semi-synthetic lipoglycopeptide derivative of vancomycin with a decylaminoethyl side chain that is active against Gram-positive bacteria including Staphylococcus aureus strains resistant to methicillin or vancomycin. This study describes transcriptome alterations in S. aureus strain ATCC29213 treated with telavancin for 15 min and 60 min in comparing with other agents treatment, including vancomycin, enduracidin, m-chlorophenylhydrazone.

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Potential Mechanism of Action of 3'-Demethoxy-6-O-Demethylisoguaiacin on Methicillin-resistant Staphylococcus aureus

Project description:Methicillin-resistant Staphylococcus aureus is one of the major causative agents associated to infections with a high morbidity and mortality in hospitals worldwide. In previous studies, we reported that lignan 3'-demethoxy-6-O-demethylisoguaiacin isolated and characterized from Larrea tridentata showed the best activity towards methicillin-resistant S. aureus. Understanding of mechanism of action of drugs allows design drugs in a better way. Therefore, we employed microarray to obtain gene expression profile of methicillin-resistant S. aureus after exposure to 3'-demethoxy-6-O-demethylisoguaiacin. The results showed that lignan had an effect on cell membrane affecting proteins of the ATP-binding cassette (ABC) transport system causing bacteria death. This study consisted of comparison of isolated RNA of MRSA not treated and MRSA treated with lignan 3'-demethoxy-6-O-demethylisoguaiacin. Both RNAs samples were differentially dyed with Cy3 and Cy5 during cDNA synthesis and hybridized on DNA chip. Afterwards, the chip was scanned in a GenePix 4000B scanner. The resulting gene expression profile was analyzed in databases for functional annotations to find a potential mechanism of the lignan in MRSA.

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Project description:Methicillin-resistant Staphylococcus aureus (MRSA) is a major hospital- and community-acquired pathogen, but the mechanisms underlying host-defense to MRSA remain poorly understood. Here, we investigated the role of IL-21 in this process. When administered intra-tracheally into wild-type mice, IL-21 induced granzymes and augmented clearance of pulmonary MRSA but not when neutrophils were depleted or a granzyme B inhibitor was added. Correspondingly, IL-21 induced MRSA killing by human peripheral blood neutrophils. Unexpectedly, however, basal MRSA clearance was enhanced when IL-21 signaling was blocked, both in Il21r KO mice and in wild-type mice injected with IL-21R-Fc fusion-protein. This correlated with increased type I interferon and an IFN-related gene signature, and indeed anti-IFNAR1 treatment diminished MRSA clearance in these animals. Moreover, we found that IFNβ induced granzyme B and promoted MRSA clearance in a granzyme B-dependent fashion. These results reveal an interplay between IL-21 and type-I IFN in the innate immune response to MRSA.

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Project description:Methicillin-resistant Staphylococcus aureus

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