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MRSA temporal adaptation to the healthy and influenza injured lung microenvironment

ABSTRACT: MRSA temporal adaptation to the healthy and influenza injured lung microenvironment

PROVIDER: PRJNA821217 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18521900_1.fastq.gz	Fastqsanger.gz
	SRR18521900_2.fastq.gz	Fastqsanger.gz
	SRR18521901_1.fastq.gz	Fastqsanger.gz
	SRR18521901_2.fastq.gz	Fastqsanger.gz
	SRR18521902_1.fastq.gz	Fastqsanger.gz

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MRSA temporal adaptation to the healthy and influenza injured lung microenvironment

Project description:Influenza-induced respiratory failure is substantially worsened by secondary bacterial infections such as methicillin-resistant Staphylococcus aureus (MRSA). The bidirectional interaction between the influenza-injured lung microenvironment and MRSA is poorly understood. By conditioning MRSA ex vivo in bronchoalveolar lavage (BAL) fluid collected from mice at various timepoints of influenza infection, we found that influenza-injured lung microenvironment induces MRSA to increase cytotoxin expression while decreasing metabolic pathways. This overall increase in MRSA virulence was dependent upon SaeRS, a bacterial two-component system. Once expressed by MRSA, these influenza-induced toxins (such as Hla and LukAB) interact with host heparan sulfate (HS) fragments shed into the airspace. Highly-sulfated HS fragments augmented Hla- and LukAB-toxicity in vitro and in vivo. Our findings indicate that post-influenza MRSA pneumonia is shaped by bidirectional host-pathogen interactions: host injury triggers changes in bacterial expression of toxins, the activity of which are then shaped by host-derived HS fragments.

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The influenza-injured lung microenvironment promotes MRSA virulence, contributing to severe secondary bacterial pneumonia.

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