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Staphylococcus aureus gene expression in a rat model of infective endocarditis

ABSTRACT: S. aureus has a propensity to cause endocarditis; diabetes mellitus is a frequent underlying comorbitity in patents with S. aureus endocarditis. S. aureus Affymetrix GeneChips were used to compare S. aureus expression properties in cardiac vegatations isolated from diabetic and nondiabetic rats. S. aureus Affymetrix GeneChips were also used to compare the S. aureus expression properties of cardiac vegatations (both diabetic and nondiabetic) in comparsions to planktonic cells. Few differences were observed between the expression properties of S. aureus harvested from diabetic vs. nondiabetic cardiac vegatations. Significant differences were observed between the expression properties of S. aureus harvested from cardiac vegetations in comparison to exponential and/or stationary phase planktonically grown cells.

ORGANISM(S): Staphylococcus aureus

PROVIDER: GSE62390 | GEO | 2014/11/01

SECONDARY ACCESSION(S): PRJNA263999

REPOSITORIES: GEO

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Project description:Tax1-binding protein 1 (Tax1bp1) negatively regulates NF-κB by editing the ubiquitylation of target molecules with its catalytic partner A20. Genetically engineered TAX1BP1-deficient (KO) mouse develops age-dependent inflammatory constitution in multiple organs including heart, liver, skin and succumb to premature heart failure. Laser capture dissection and gene expression microarray analysis on the mitral valves of TAX1BP1-KO mice (8 and 16 week old) revealed that the 588 transcription alterations. SAA3 (serum amyloid A3), at 1,180-fold induction (FI), CHI3L1(361-FI), HP(187-FI), IL1B(122-FI) and SPP1/OPN(101-FI) and WIF1 (Wnt inhibitory factor 1) at 11-fold decrease implied extensive inflammation and tissue degeneration at this microenvironment. Intense Saa3 staining and significant reduction of I-κBα at the same area, massive infiltration of inflammatory lymphocytes and edema formation at the peripheral areas of sinoatrial and atrioventricular node were also observed and electrocardiogram indicated atrioventricular conduction defect (elongated PQ-interval) in TAX1BP1-KO mice. Since antibiotics-induced ‘germ free’ status for three months significantly ameliorated these chronic autoimmune and altered cardiac excitation properties, we conclude that these chronic pathological conditions, as we named ‘pseudo-infective endocarditis’ were boosted by the commensal microbiota those who are usually harmless by their nature. This experimental outcome raises a novel mechanistic linkage between endothelial inflammation and cardiac dysfunction. We employed laser capture microdissection (LCM) and gene expression microarray technique to obtain the specific gene expression information of pathologic organ. Total RNAs of mitral valves from three independent tissues of 8- or 16-week age (-wk) male mice of either WT or TAX1BP1-KO mice were prepared by LCM followed by total RNA extraction kit. Then the global mRNA expression profiles were analyzed by Agilent gene expression microarray.

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Staphylococcus aureus gene expression in a rat model of infective endocarditis

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