Abstract
Porcine pleuropneumonia is a highly contagious respiratory disease that causes great economic losses worldwide. In this study, we aimed to explore the underlying relationship between infection and injury by investigation of the whole porcine genome expression profiles of swine lung tissues post-inoculated with experimentally Actinobacillus pleuropneumoniae. Expression profiling experiments of the control group and the treatment group were conducted using a commercially available Agilent Porcine Genechip including 43,603 probe sets. Microarray analysis was conducted on profiles of lung from challenged versus non-challenged swine. We found 11,929 transcripts, identified as differentially expressed at the p ≤0.01 level. There were 1188 genes annotated as swine genes in the GenBank Data Base. GO term analysis identified a total of 89 biological process categories, 82 cellular components and 182 molecular functions that were significantly affected, and at least 27 biological process categories that were related to the host immune response. Gene set enrichment analysis identified 13 pathways that were significantly associated with host response. Many proinflammatory-inflammatory cytokines were activated and involved in the regulation of the host defense response at the site of inflammation; while the cytokines involved in regulation of the host immune response were suppressed. All changes of genes and pathways of induced or repressed expression not only led to a decrease in antigenic peptides presented to T lymphocytes by APCs via the MHC and alleviated immune response injury induced by infection, but also stimulated stem cells to produce granulocytes (neutrophils, eosinophils, and basophils) and monocyte, and promote neutrophils and macrophages to phagocytose bacterial and foreign antigen at the site of inflammation. The defense function of swine infection with Actinobacillus pleuropneumoniae was improved, while its immune function was decreased.
Highlights
Porcine pleuropneumonia (PP) is a highly contagious respiratory disease that causes great economic losses worldwide [1]
We found that: (1) A total of 89 biological process categories, 82 cellular components and 182 molecular functions were significantly affected, and more than 27 biological process were involved in the host immune response; (2) At the site of inflammation, 13 pathways associated with host responses were affected significantly; many proinflammatory-inflammatory cytokines were activated and several immunomodulatory cytokines were suppressed at the gene expression level reflecting the complex machinery at work during an infection; (3) Many genes which were involved in a variety of cellular functions-proliferation, differentiation, growth arrest or apoptosis of normal cells that activated, could stimulate stem cells to produce granulocyte and monocyte
We have identified a set of differentially expressed (DE) genes in our current case-control study, and a functional enrichment analysis indicated that these DE genes mainly related to “host immune response” and “host response”
Summary
Porcine pleuropneumonia (PP) is a highly contagious respiratory disease that causes great economic losses worldwide [1]. Actinobacillus pleuropneumoniae (APP) is the causative agent of PP and can spread quickly by air-borne particles and/or touching a contaminated surface, and often kills infected animals in the acute phase when extensive lung hemorrhage and necrosis occur. Using cDNA microarrays, Moser and co-workers found 307 anonymous transcripts in blood leukocytes from swine that were significantly affected by experimental infection with APP [5]. Hedegaard et al investigated the molecular characterization of the early response in pigs to experimental infection with APP serotype 5B, using cDNA microarrays [6]. Two-colour microarray analysis was conducted to identify genes being significantly differently expressed in non-inflamed lung tissue compared with inflamed lung tissue sampled from the same animal [6]. Mortensen et al studied the local transcriptional response in different locations of lung from pigs experimentally infected with the respiratory pathogen
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