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    MicroRNA regulation of bovine monocyte inflammatory and metabolic networks in an in vivo infection model.

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    Author
    Lawless, Nathan
    Reinhardt, Timothy A.
    Bryan, Kenneth
    Baker, Mike
    Pesch, Bruce
    Zimmerman, Duane
    Zuelke, Kurt
    Sonstegard, Tad
    O'Farrelly, Cliona
    Lippolis, John D.
    Lynn, David J.
    Keyword
    Infection
    Innate immunity
    RNAseq
    Transcriptional networks
    MicroRNA
    Complex genetics
    Tolerance
    Complex immunity
    Resistance
    Date
    2014-01-27
    
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    URI
    http://hdl.handle.net/11019/799; http://dx.doi.org/10.1534/g3.113.009936
    Citation
    Nathan Lawless, Timothy A. Reinhardt, Kenneth Bryan, Mike Baker, Bruce Pesch, Duane Zimmerman, Kurt Zuelke, Tad Sonstegard, Cliona O'Farrelly, John D. Lippolis and David J. Lynn. MicroRNA Regulation of Bovine Monocyte Inflammatory and Metabolic Networks in an In Vivo Infection Model. G3: Genes|Genomes|Genetics published on January 27, 2014 as doi:10.1534/g3.113.009936
    Abstract
    Bovine mastitis is an inflammation-driven disease of the bovine mammary gland that costs the global dairy industry several billion dollars per annum. Because disease susceptibility is a multi-factorial complex phenotype, an integrative biology approach is required to dissect the molecular networks involved. Here, we report such an approach, using next generation sequencing combined with advanced network and pathway biology methods to simultaneously profile mRNA and miRNA expression at multiple time-points (0, 12, 24, 36 and 48h) in both milk and blood FACS-isolated CD14+ monocytes from animals infected in vivo with Streptococcus uberis. More than 3,700 differentially expressed (DE) genes were identified in milk-isolated monocytes (MIMs), a key immune cell recruited to the site of infection during mastitis. Up-regulated genes were significantly enriched for inflammatory pathways, while down-regulated genes were enriched for non-glycolytic metabolic pathways. Monocyte transcriptional changes in the blood, however, were more subtle but highlighted the impact of this infection systemically. Genes up-regulated in blood-isolated-monocytes (BIMs) showed a significant association with interferon and chemokine signalling. Furthermore, twenty-six miRNAs were differentially expressed in MIMs and three in BIMs. Pathway analysis revealed that predicted targets of down-regulated miRNAs were highly enriched for roles in innate immunity (FDR < 3.4E-8) in particular TLR signalling, while up-regulated miRNAs preferentially targeted genes involved in metabolism. We conclude that during S. uberis infection miRNAs are key amplifiers of monocyte inflammatory response networks and repressors of several metabolic pathways.
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