Trimeric autotransporter adhesins contribute to Actinobacillus pleuropneumoniae pathogenicity in mice and regulate bacterial gene expression during interactions between bacteria and porcine primary alveolar macrophages
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  • 作者:Wanhai Qin ; Lei Wang ; Ruidong Zhai ; Qiuyue Ma ; Jianfang Liu
  • 关键词:Actinobacillus pleuropneumoniae ; Trimeric autotransport adhesin ; Gene expression profiles
  • 刊名:Antonie van Leeuwenhoek
  • 出版年:2016
  • 出版时间:January 2016
  • 年:2016
  • 卷:109
  • 期:1
  • 页码:51-70
  • 全文大小:1,301 KB
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  • 作者单位:Wanhai Qin (1)
    Lei Wang (1) (2)
    Ruidong Zhai (1)
    Qiuyue Ma (1)
    Jianfang Liu (1)
    Chuntong Bao (1)
    Hu Zhang (3)
    Changjiang Sun (1)
    Xin Feng (1)
    Jingmin Gu (1)
    Chongtao Du (1)
    Wenyu Han (1)
    P. R. Langford (4)
    Liancheng Lei (1)

    1. College of Veterinary Medicine, Jilin University, Changchun, People’s Republic of China
    2. College of Animal Science, Henan Institute of Science and Technology, Xinxiang, People’s Republic of China
    3. School of Public Health, Jilin University, Changchun, People’s Republic of China
    4. Section of Paediatrics, Imperial College London, London, UK
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciences
    Microbiology
    Medical Microbiology
    Plant Sciences
    Soil Science and Conservation
  • 出版者:Springer Netherlands
  • ISSN:1572-9699
文摘
Actinobacillus pleuropneumoniae is an important pathogen that causes respiratory disease in pigs. Trimeric autotransporter adhesin (TAA) is a recently discovered bacterial virulence factor that mediates bacterial adhesion and colonization. Two TAA coding genes have been found in the genome of A. pleuropneumoniae strain 5b L20, but whether they contribute to bacterial pathogenicity is unclear. In this study, we used homologous recombination to construct a double-gene deletion mutant, ΔTAA, in which both TAA coding genes were deleted and used it in in vivo and in vitro studies to confirm that TAAs participate in bacterial auto-aggregation, biofilm formation, cell adhesion and virulence in mice. A microarray analysis was used to determine whether TAAs can regulate other A. pleuropneumoniae genes during interactions with porcine primary alveolar macrophages. The results showed that deletion of both TAA coding genes up-regulated 36 genes, including ene1514, hofB and tbpB2, and simultaneously down-regulated 36 genes, including lgt, murF and ftsY. These data illustrate that TAAs help to maintain full bacterial virulence both directly, through their bioactivity, and indirectly by regulating the bacterial type II and IV secretion systems and regulating the synthesis or secretion of virulence factors. This study not only enhances our understanding of the role of TAAs but also has significance for those studying A. pleuropneumoniae pathogenesis.

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