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Phenotypic and genotypic characteristics of MSSA isolates responsible for infective endocarditis

ABSTRACT: Phenotypic and genotypic characteristics of MSSA isolates responsible for infective endocarditis

PROVIDER: PRJEB82234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13933400_1.fastq.gz	Fastqsanger.gz
	ERR13933400_2.fastq.gz	Fastqsanger.gz
	ERR13933401_1.fastq.gz	Fastqsanger.gz
	ERR13933401_2.fastq.gz	Fastqsanger.gz
	ERR13933402_1.fastq.gz	Fastqsanger.gz

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Project description:Background—Diagnosis and pronostic assessment are challenging in infective endocarditis (IE). To investigate the host response during IE and identify potential biomarkers, we determined the circulating gene expression profile through a whole genome microarray analysis. Methods and Results—A transcriptomic case-control study was performed on blood samples from patients with native valve IE (n=39), excluded IE after an initial suspicion (n=10) at patient’s admission, and age-matched healthy controls (n=10). The whole genome microarray analysis showed that patients with IE exhibited a specific transcriptional program with a predominance of gene categories associated with cell activation, innate immune and inflammatory responses. These categories were organized in a dense network from which arose numerous subnetworks including major histocompatibily complex and natural killer cell network, type 1 interferon pathway and intracellular traffic. Quantitative real-time RT-PCR performed on a selection of highly modulated genes showed that the expression of the gene encoding S100 calcium binding protein A11 (S100A11) was significantly increased in patients with IE in comparison with controls (P<0.001) and patients with excluded IE (P<0.05). Interestingly, the upregulated expression of S100A11 gene was more pronounced in staphylococcal IE than in streptococcal IE (P<0.01). These results were confirmed by serum concentrations of the S100A11 protein. Finally, we showed that, in patients with IE, the upregulation of aquaporin-9 gene (AQP9) was significantly related to the occurrence of acute heart failure (P=0.02). Conclusions— Using transcriptional signatures of blood samples, we identified S100A11 as a potential diagnostic marker of IE. In addition, the determination of AQP9 may improve the prognostic assessment of IE.

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