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    Mapping epigenetic changes to the host cell genome induced by Burkholderia pseudomallei reveals pathogen-specific and pathogen-generic signatures of infection.

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    URI
    http://hdl.handle.net/11287/620271
    Author
    Cizmeci, D.
    Dempster, E. L.
    Champion, O. L.
    Wagley, S.
    Akman, O. E.
    Prior, J. L.
    Soyer, O. S.
    Mill, Jonathan
    Titball, R. W.
    Date
    2016-08-03
    Journal
    Scientific reports
    Type
    Journal Article
    Publisher
    Nature
    DOI
    10.1038/srep30861
    Rights
    Archived with thanks to Scientific reports
    Metadata
    Show full item record
    Abstract
    The potential for epigenetic changes in host cells following microbial infection has been widely suggested, but few examples have been reported. We assessed genome-wide patterns of DNA methylation in human macrophage-like U937 cells following infection with Burkholderia pseudomallei, an intracellular bacterial pathogen and the causative agent of human melioidosis. Our analyses revealed significant changes in host cell DNA methylation, at multiple CpG sites in the host cell genome, following infection. Infection induced differentially methylated probes (iDMPs) showing the greatest changes in DNA methylation were found to be in the vicinity of genes involved in inflammatory responses, intracellular signalling, apoptosis and pathogen-induced signalling. A comparison of our data with reported methylome changes in cells infected with M. tuberculosis revealed commonality of differentially methylated genes, including genes involved in T cell responses (BCL11B, FOXO1, KIF13B, PAWR, SOX4, SYK), actin cytoskeleton organisation (ACTR3, CDC42BPA, DTNBP1, FERMT2, PRKCZ, RAC1), and cytokine production (FOXP1, IRF8, MR1). Overall our findings show that pathogenic-specific and pathogen-common changes in the methylome occur following infection.
    Citation
    Mapping epigenetic changes to the host cell genome induced by Burkholderia pseudomallei reveals pathogen-specific and pathogen-generic signatures of infection. 2016, 6:30861 Sci Rep
    Publisher URL
    http://dx.doi.org/10.1038/srep30861
    Note
    This article is freely available. Click on the Additional Link above to access the full-text.
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