4.3 Article

Hepatic gene expression changes in pigs experimentally infected with the lung pathogen Actinobacillus pleuropneumoniae as analysed with an innate immunity focused microarray

Journal

INNATE IMMUNITY
Volume 16, Issue 6, Pages 343-353

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1177/1753425909342730

Keywords

acute phase protein; hepatic transcriptional response; innate defence; gene expression; pig

Funding

  1. Danish Research Council [274-07-0389]

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Knowledge on gene expression in the liver during respiratory infections is limited although it is well-established that this organ is an important site of synthesis of several systemic innate immune components as response to infections. In the present study, the early transcriptional hepatic response of genes associated with innate immune responses was studied in pigs 14-18 h after intranasal inoculation with Actinobacillus pleuropneumoniae, using innate immune focused microarrays and quantitative real-time PCR (qPCR). The microarray analysis of liver tissue established that 51 genes were differentially expressed. A large group of these genes encoded proteins involved in the acute phase response, including serum amyloid A, C-reactive protein, fibrinogen, haptoglobin and tumor necrosis factor-alpha the expression of which were all found to be up-regulated and glutathione S-transferase, transthyretin, transferrin and albumin which were down-regulated. Additional genes associated with innate immune responses were investigated using qPCR; genes encoding interleukin-(IL-)1, IL-6, IL-8, lipopolysaccharide binding protein, lactotransferrin, and PigMAP were up-regulated and interferon 1 alpha, alpha(1)-acid glycoprotein, mannan-binding lectin A, surfactant protein D, and surfactant protein Al were down-regulated in the liver of infected animals. Down-regulation of alpha(1)-acid glycoprotein during infection has not been described previously in any species. These results confirm that the liver plays an important role in initiating and orchestrating the innate immune response to A. pleuropneumoniae infection.

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