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Histone H3 Acetylation and microRNA(s) Regulate Inflammatory response in Mastitis Mice, induced by Staphylococcus aureus Infection

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE54232 | GEO | 2014/06/01

SECONDARY ACCESSION(S): PRJNA235991

REPOSITORIES: GEO

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Histone H3 Acetylation and microRNA(s) Regulate Inflammatory response in Mastitis Mice, induced by Staphylococcus aureus Infection

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-01 | E-GEOD-54232 | biostudies-arrayexpress

Histone H3 Acetylation and microRNA(s) Regulate Inflammatory response in Mastitis Mice, induced by Staphylococcus aureus Infection [Microarray]

Project description:Bacterial infection in the mammary gland parenchyma induces local inflammation that can lead to a multietiological complex disease called mastitis. Globally Staphylococcus aureus is the single largest mastitis pathogen and the infection can ultimately result in either subclinical or chronic and sometimes lifelong infection. In the present report we have addressed the differential inflammatory response in the mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus. Immunohistochemical and immunoblot analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Real-time PCR and genome-wide gene expression studied showed expression of a set of proinflammatory genes and cytokines in a temporal manner. Remarkably, over expression of the genes significantly correlated with the promoter specific acetylation in these residues. Furthermore, we have identified several differentially expressed known miRNAs and 4 novel miRNAs in the S. aureus infected mice mammary tissue by small RNA sequencing. By employing these gene expression data, an attempt has been made to delineate the gene regulatory networks in the strain specific inflammatory response. Apparently, one of the isolates of S. aureus activated the NFkB signaling leading to drastic inflammatory response and induction of immune surveillance, which could lead to rapid clearance of the pathogen. The other strain repressed most of the inflammatory response, which might help in its sustenance in the host tissue. Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis. 3 samples in two biological replicates. One control and two samples infected with two different strains of S. aureus

2014-06-01 | E-GEOD-54230 | biostudies-arrayexpress

Histone H3 Acetylation and microRNA(s) Regulate Inflammatory response in Mastitis Mice, induced by Staphylococcus aureus Infection [Microarray]

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Histone H3 Acetylation and microRNA(s) Regulate Inflammatory response in Mastitis Mice, induced by Staphylococcus aureus Infection [smallRNA-Seq]

Project description:Bacterial infection in the mammary gland parenchyma induces local inflammation that can lead to a multietiological complex disease called mastitis. Globally Staphylococcus aureus is the single largest mastitis pathogen and the infection can ultimately result in either subclinical or chronic and sometimes lifelong infection. In the present report we have addressed the differential inflammatory response in the mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus. Immunohistochemical and immunoblot analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Real-time PCR and genome-wide gene expression studied showed expression of a set of proinflammatory genes and cytokines in a temporal manner. Remarkably, over expression of the genes significantly correlated with the promoter specific acetylation in these residues. Furthermore, we have identified several differentially expressed known miRNAs and 4 novel miRNAs in the S. aureus infected mice mammary tissue by small RNA sequencing. By employing these gene expression data, an attempt has been made to delineate the gene regulatory networks in the strain specific inflammatory response. Apparently, one of the isolates of S. aureus activated the NFkB signaling leading to drastic inflammatory response and induction of immune surveillance, which could lead to rapid clearance of the pathogen. The other strain repressed most of the inflammatory response, which might help in its sustenance in the host tissue. Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis. One control and two samples infected with two different strains of S. aureus

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Histone H3 Acetylation and microRNA(s) Regulate Inflammatory response in Mastitis Mice, induced by Staphylococcus aureus Infection [smallRNA-Seq]

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