Please use this identifier to cite or link to this item: http://lib.jncasr.ac.in:8080/jspui/handle/10572/2330
Title: Epigenetic response in mice mastitis: Role of histone H3 acetylation and microRNA(s) in the regulation of host inflammatory gene expression during Staphylococcus aureus infection
Authors: Modak, Rahul
Das Mitra, Susweta
Vasudevan, Madavan
Krishnamoorthy, Paramanandhan
Kumar, Manoj
Bhat, Akshay V.
Bhuvana, Mani
Ghosh, Sankar K.
Shome, Bibek R.
Kundu, Tapas Kumar
Keywords: Oncology
Epigenetic Modifications
Histone
Acetylation
Mastitis
S. Aureus Infection
Micro-RNA
Gene Expression
Inflammatory Response
Chromatin Immunoprecipitation
Mammary Epithelial-Cells
Escherichia-Coli
Blood-Cells
Mouse
Gland
Relevance
Pathogens
Cytokine
Promoter
Issue Date: 2014
Publisher: Biomed Central Ltd
Citation: Modak, R; Das Mitra, S; Vasudevan, M; Krishnamoorthy, P; Kumar, M; Bhat, AV; Bhuvana, M; Ghosh, SK; Shome, BR; Kundu, TK, Epigenetic response in mice mastitis: Role of histone H3 acetylation and microRNA(s) in the regulation of host inflammatory gene expression during Staphylococcus aureus infection. Clinical Epigenetics 2014, 6, 12 http://dx.doi.org/10.1186/1868-7083-6-12
Clinical Epigenetics
6
Abstract: Background: There is renewed interest towards understanding the host-pathogen interaction in the light of epigenetic modifications. Although epithelial tissue is the major site for host-pathogen interactions, there is handful of studies to show how epithelial cells respond to pathogens. Bacterial infection in the mammary gland parenchyma induces local and subsequently systemic inflammation that results in a 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. Results: In the present report we have addressed the differential inflammatory response in mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus, isolated from field samples. Immunohistochemical and immunoblotting analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Global gene expression analysis in S. aureus infected mice mammary tissue revealed a selective set of upregulated genes that significantly correlated with the promoter specific, histone H3K14 acetylation. Furthermore, we have identified several differentially expressed known miRNAs and 3 novel miRNAs in 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 NF-kB signaling leading to drastic inflammatory response and induction of immune surveillance, which could possibly 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. Conclusion: Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis. In a broader perspective this study also paves the way to understand how certain bacteria can evade the immune surveillance and cause sustained infection while others are rapidly cleared from the host body.
Description: Open Access
URI: http://hdl.handle.net/10572/2330
ISSN: 1868-7083
Appears in Collections:Research Papers (Tapas K. Kundu)

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